Autoimmunity: Mechanisms and Veterinary Examples

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-08-11

Key Takeaways

• Autoimmune disease arises from a breakdown in central and peripheral self-tolerance mechanisms, allowing autoreactive T and B lymphocytes to persist and attack self-antigens, leading to tissue injury via effector pathways such as antibody-mediated cytotoxicity (Type II hypersensitivity) or immune complex deposition (Type III hypersensitivity).
• Genetic predisposition, often polygenic and involving MHC and non-MHC loci, contributes significantly to autoimmune risk, as exemplified by breed predispositions in dogs for conditions like immune-mediated hemolytic anemia (IMHA) and immune-mediated polyarthritis (IMPA).
• Environmental triggers, including viral infections that can induce molecular mimicry, bystander activation, or epitope spreading, are implicated in initiating or exacerbating autoimmunity, though definitive causal links in individual veterinary patients are often inferential.
• The diagnostic approach for suspected autoimmune disease necessitates a structured sequence: confirming immune-mediated inflammation (e.g., spherocytes/positive Coombs test in IMHA, inflammatory synovial fluid in IMPA), excluding infectious and neoplastic mimics, and identifying the target tissue or cell line to guide prognosis and monitoring.
• Effector mechanisms, such as the IL-23-IL-17 axis driving chronic inflammation in IMPA or autoantibodies mediating erythrocyte destruction in IMHA, dictate the histopathologic patterns and inform the selection of diagnostic tests and monitoring parameters.
• Antemortem confirmation of autoimmune disease is achievable with validated autoantibody assays (e.g., acetylcholine receptor antibodies for myasthenia gravis), but many veterinary conditions remain presumptive, relying on exclusion of differentials and response to immunosuppressive therapy.

Autoimmune disease arises when the immune system directs a sustained, targeted response against self-antigens, causing tissue injury that mirrors the effector mechanisms used against pathogens. This article explains how self-tolerance fails at the central and peripheral checkpoints, how genetic and environmental factors converge to trigger disease, and how these principles manifest across domestic species. It is written for veterinary students who already understand basic immunology and clinical pathology, and it answers a specific question: given a patient with suspected immune-mediated disease, what mechanistic framework should guide interpretation of the clinical signs, laboratory findings, and histopathology?

The article draws on comparative immunology, spontaneous animal models, and induced experimental systems. It covers the major tolerance checkpoints, the effector pathways that execute tissue damage, the role of infection and molecular mimicry, and the clinical syndromes most relevant to veterinary practice, including immune-mediated hemolytic anemia and immune-mediated polyarthritis. Treatment is excluded by design, the companion article on therapeutic decision-making addresses that topic.

At a Glance

Central Tolerance and Its Failure

Central tolerance operates in primary lymphoid organs. In the thymus, developing T cells that bind self-peptide-MHC complexes with high affinity undergo negative selection and apoptosis. Medullary thymic epithelial cells express tissue-restricted antigens under the control of the autoimmune regulator gene, ensuring that many peripheral proteins are visible to the developing T cell repertoire. In the bone marrow, immature B cells encountering high-avidity self-antigen are deleted or undergo receptor editing.

The non-obese diabetic (NOD) mouse illustrates how central tolerance defects contribute to organ-specific autoimmunity. This strain develops spontaneous autoimmune diabetes with pancreas-specific autoantibodies and autoreactive CD4+ and CD8+ T cells, and its genetic architecture includes multiple susceptibility loci that impair both central and peripheral tolerance mechanisms. The NOD mouse as a model of immune dysregulation has been instrumental in showing that no single tolerance failure suffices to cause disease, rather, the summation of several defective checkpoints is required.

Peripheral Tolerance and Its Breakdown

Peripheral tolerance mechanisms restrain self-reactive lymphocytes that escape the thymus and bone marrow. These include clonal anergy, deletion by activation-induced cell death, and active suppression by regulatory T cells. Immunologic ignorance, in which self-antigens are sequestered behind anatomical barriers or presented at too low a density to activate T cells, also operates in sites such as the central nervous system and the anterior chamber of the eye.

B Cell Survival and the BAFF System

B cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL) are TNF family members that promote peripheral B cell survival. Excess BAFF drives accumulation of autoreactive B cells that would normally be eliminated. In mouse models, BAFF overexpression produces autoimmune manifestations resembling systemic lupus erythematosus, and elevated serum BAFF is found in human patients with several autoimmune conditions. The review of BAFF biology proposes that BAFF-induced autoimmunity may arise from T cell-independent B cell activation instead of a global collapse of B cell tolerance, a distinction with therapeutic implications because BAFF-depleting agents target this survival pathway.

Regulatory T Cell Function

Regulatory T cells suppress effector responses through contact-dependent mechanisms and cytokine secretion. Their failure, whether by reduced numbers, impaired function, or resistance of effector cells to suppression, permits expansion of autoreactive clones. The relative contribution of regulatory T cell dysfunction varies by disease and by species, and in many veterinary syndromes the precise defect has not been characterized.

Effector Mechanisms of Tissue Injury

Once tolerance fails, the effector phase determines the clinical and pathologic phenotype. Autoantibodies against cell surface or matrix antigens produce type II hypersensitivity, exemplified by immune-mediated hemolytic anemia, in which opsonized erythrocytes are destroyed by phagocytosis or complement-mediated lysis. Immune complex deposition produces type III hypersensitivity, as seen in some glomerulonephritides and vasculitides. Autoreactive T cells mediate direct cytotoxicity or recruit macrophages through interferon-gamma secretion.

The IL-23-IL-17 Axis

The discovery of the IL-23-IL-17 pathway revised the understanding of T helper subsets in autoimmunity. Th17 cells and other IL-17-producing cells, including innate lymphoid cells and gamma-delta T cells, contribute to chronic inflammatory arthritis. The review of the IL-23-IL-17 axis in inflammatory arthritis notes that cells expressing the IL-23 receptor become pathogenic after exposure to IL-23, but the timing, location, and relative contribution of each IL-17-producing population remain incompletely defined. This pathway is relevant to immune-mediated polyarthritis in dogs, where synovial inflammation with neutrophilic or lymphoplasmacytic infiltrates reflects cytokine-driven recruitment instead of direct autoantibody-mediated injury.

T Cell Subsets in Organ-Specific Disease

In the central nervous system, autoreactive CD4+ T cells of both Th1 and Th17 lineages can mediate demyelinating disease, and myelin-specific CD8+ T cells also contribute in experimental models. The review of autoimmune T cell responses in the CNS emphasizes that the interplay between these subsets influences pathology and clinical course. Antigen presenting cells within the CNS, including microglia and astrocytes, perpetuate inflammation by presenting myelin epitopes and secreting inflammatory factors, as described in the review of antigen presenting cells in multiple sclerosis. These mechanisms have direct parallels in canine granulomatous meningoencephalomyelitis, although the specific autoantigens remain unidentified.

Environmental Triggers and Molecular Mimicry

Infections are the most studied environmental trigger for autoimmunity. Epidemiological and experimental evidence implicates enteric viruses such as Coxsackie B virus and rotavirus, influenza A viruses, and herpesviruses in the induction or protection from autoimmune disease, depending on genetic background, viral strain, viral load, and timing of infection. The review of viruses and autoimmunity identifies four principal mechanisms: molecular mimicry, in which viral epitopes cross-react with self-antigens, epitope spreading, in which tissue damage releases novel self-epitopes that broaden the response, bystander activation of pre-existing autoreactive cells, and immortalization of infected B cells. The evidence for these mechanisms in spontaneous veterinary disease is largely inferential, and definitive causal links are rarely established in individual patients.

Genetic Architecture and Breed Predisposition

Autoimmune risk is polygenic. MHC haplotypes determine which self-peptides are presented and therefore shape the autoreactive T cell repertoire. Non-MHC loci influence cytokine production, regulatory T cell function, and target organ susceptibility. The NOD mouse again provides the reference framework, with disease requiring the summation of multiple defective tolerance mechanisms instead of a single mutation. Breed predispositions in dogs, such as the overrepresentation of certain breeds for immune-mediated hemolytic anemia and immune-mediated polyarthritis, are consistent with polygenic inheritance, but specific risk alleles are largely uncharacterized in veterinary species.

Diagnostic Approach to Suspected Autoimmune Disease

The clinical diagnosis of autoimmune disease rests on a structured sequence: confirm immune-mediated inflammation, exclude infectious and neoplastic mimics, identify the target tissue or cell line, and then characterize the mechanism where this changes management. This sequence applies across species, but the order and urgency of steps differ with the presentation.

Step 1: Confirm Immune-Mediated Inflammation

The first decision is whether the lesion or cytopenia is truly immune-mediated. For immune-mediated hemolytic anemia (IMHA), the finding of spherocytes, autoagglutination, or a positive direct antiglobulin (Coombs) test supports an antibody-mediated process. For immune-mediated polyarthritis (IMPA), the demonstration of suppurative inflammation in synovial fluid with a negative culture is the central finding. In both syndromes, the key differentials are infection, neoplasia, and drug reactions.

The diagnostic threshold matters. A positive antiglobulin test in an anemic dog with spherocytes is strong support for IMHA. A negative test does not exclude it, particularly when glucocorticoids have already been given or when the antibody load is low. In cats, autoagglutination must be distinguished from rouleaux by the saline dilution test, since feline red cells aggregate readily.

Step 2: Exclude Infection and Neoplasia

Infectious agents can trigger or mimic autoimmune disease. The mechanisms include molecular mimicry, bystander activation, and epitope spreading, as reviewed in the literature on viral triggers of autoimmunity (viral-induced autoimmunity mechanisms). In endemic regions, vector-borne diseases such as ehrlichiosis, anaplasmosis, and babesiosis must be excluded before committing to immunosuppressive therapy. The same applies to feline leukemia virus and feline immunodeficiency virus in cats, and to retroviral testing in other species where relevant.

Neoplasia is the second major mimic. Paraneoplastic immune-mediated disease occurs with lymphoma, leukemia, and some carcinomas. The practical rule is that a diagnosis of primary autoimmune disease requires a reasonable search for occult neoplasia, particularly in middle-aged and older animals. Thoracic radiographs, abdominal ultrasound, and lymph node cytology are part of this search in dogs and cats. In horses and cattle, the search is guided by signalment, production system, and the presenting syndrome.

Step 3: Identify the Target and Mechanism

Once immune-mediated disease is confirmed, the target tissue or cell line defines the syndrome. The mechanism matters for prognosis and monitoring. Type II cytotoxic antibody responses dominate in IMHA and immune-mediated thrombocytopenia. Type III immune complex deposition underlies many glomerulonephritides and some vasculitides. Type IV T cell-mediated mechanisms drive diseases such as lymphocytic plasmacytic enteritis and many endocrinopathies, including lymphocytic thyroiditis.

The distinction between primary and secondary autoimmune disease is clinically important. Secondary forms carry a better prognosis when the trigger is removed. The NOD mouse model illustrates how multiple defective tolerance mechanisms summate to produce disease, and the same principle applies in clinical patients (tolerance breakdown in the NOD mouse). A single animal may have more than one contributing defect, which explains why some patients relapse and others do not.

Diagnostic Decision Points

The following table summarizes the key decision points in the diagnostic sequence and the factors that change the correct choice.

Monitoring Parameters and What They Detect

Monitoring serves three purposes: detecting relapse, detecting drug toxicity, and detecting complications of the disease itself. The parameters differ by syndrome.

For IMHA, the packed cell volume, reticulocyte count, and agglutination status are the core parameters. A rising packed cell volume with a falling reticulocyte count indicates remission. A falling packed cell volume with a rising reticulocyte count indicates ongoing hemolysis or blood loss. A falling packed cell volume with a low reticulocyte count suggests bone marrow suppression, which may be drug-induced or immune-mediated.

For IMPA, the synovial fluid cell count and cytology are the definitive monitoring tools. Clinical improvement in gait and comfort is useful but lags behind synovial inflammation. The decision to taper immunosuppressive therapy should be guided by synovial fluid findings, not solely by lameness scores.

For immune-mediated skin disease, the lesion pattern and extent are the primary parameters. Repeat biopsy is rarely needed unless the disease progresses despite therapy. For immune-mediated kidney disease, the urine protein to creatinine ratio, serum creatinine, and blood pressure are the core parameters.

Species and Production System Considerations

The diagnostic approach differs by species in ways that change the correct choice.

In dogs, the autoimmune disease work-up is well standardized. The main species-specific issues are breed predispositions and the need to screen for infectious mimics. In cats, the lower incidence of classic IMHA and the higher incidence of infectious triggers shift the balance toward more extensive infectious disease testing before immunosuppression.

In horses, immune-mediated disease is often suspected on the basis of clinical signs and response to therapy, but the diagnostic tools are less validated. Synovial fluid analysis is reliable, but antiglobulin testing is less standardized. The cost of a full work-up and the value of the animal influence how far the investigation proceeds.

In cattle and other production animals, the economic context dominates. A full diagnostic work-up is rarely justified for an individual animal unless it is a valuable breeding animal. The WOAH terrestrial animal health standards provide the framework for notifiable diseases that must be excluded before a diagnosis of autoimmune disease is made. This is particularly relevant for diseases that cause similar clinical signs, such as bovine viral diarrhea virus infection.

In exotic and avian species, the evidence base is limited. The diagnostic approach is extrapolated from domestic species, but the clinician should acknowledge the uncertainty and adjust the threshold for invasive testing.

Documentation and Case Recording

The medical record should document the diagnostic sequence, the results of each test, and the reasoning behind each decision. This is not administrative burden. It is the basis for monitoring response, adjusting therapy, and defending clinical decisions if the case is reviewed.

The record should include the date and results of each diagnostic test, the infectious disease screening performed and its results, the imaging and cytology findings, and the baseline values for each monitoring parameter. The record should also document the rationale for the chosen therapy and the planned monitoring schedule.

For teaching institutions and referral practices, the Davis-Thompson Foundation veterinary pathology resources provide case material that supports pattern recognition and diagnostic reasoning. For general practitioners, the MSD Veterinary Manual professional edition provides species-specific guidance on diagnostic thresholds and interpretation. The AVMA practice resources offer professional guidance on documentation standards and practice protocols.

When the Diagnosis Remains Uncertain

A proportion of cases will not meet the diagnostic criteria for a specific autoimmune disease. The clinician then faces a choice: treat empirically, repeat tests, or refer. The correct choice depends on the severity of the disease, the cost of further investigation, and the risk of immunosuppression.

For a stable patient with mild disease, repeating tests after a short interval is reasonable. For a deteriorating patient, empirical immunosuppression may be justified after infectious disease has been reasonably excluded. For a patient with atypical features, referral to a specialist center is appropriate.

The evidence base for many veterinary autoimmune diseases is limited to case series and expert opinion. The clinician should acknowledge this uncertainty in the record and in communication with the owner. The viral-induced autoimmunity review notes that data delineating clear mechanistic interactions between infection and autoimmunity are scarce, and the same limitation applies to much of veterinary autoimmunology.

Recognized Complications and Failure Modes

Autoimmune disease in veterinary patients follows a predictable set of failure patterns. The most common is relapse after apparent remission, which usually reflects incomplete induction therapy, premature dose reduction, or an ongoing trigger that has not been eliminated. Early detection depends on serial monitoring of the original clinicopathologic abnormalities instead of on clinical appearance alone. A dog with immune-mediated hemolytic anemia may appear stable while the packed cell volume drifts downward over several days. Recheck the specific markers that defined the index episode at each revisit, and compare trends instead of single values.

A second failure mode is treatment-associated injury. Immunosuppressive doses of glucocorticoids produce iatrogenic hyperadrenocorticism, pancreatitis, and gastrointestinal ulceration. Cytotoxic agents add the risks of myelosuppression, hepatotoxicity, and sterile hemorrhagic cystitis. These complications can obscure the distinction between drug side effects and disease progression. The discriminating question is whether the new abnormality responds to dose adjustment or to additional immunosuppression. Neutropenia with fever after a cyclophosphamide pulse is drug effect until proven otherwise, and the appropriate response is dose reduction and supportive care, not escalation of immunosuppression.

A third pattern is the emergence of a second immune-mediated disease. Polyendocrine syndromes, immune-mediated hemolytic anemia followed by immune-mediated thrombocytopenia, and inflammatory arthritis with concurrent immune-mediated skin disease all occur. This is not treatment failure in the strict sense, but it changes the monitoring plan and the prognosis. The MSD Veterinary Manual provides species-specific guidance on the recognized associations and their expected timelines MSD Veterinary Manual professional reference.

Common Errors and Corrective Actions

Less experienced clinicians frequently mistake the presence of inflammation for the presence of autoimmunity. Neutrophilic inflammation in a joint, lymphocytic infiltration in a liver biopsy, or proteinuria with an active sediment all warrant a search for infection, neoplasia, or drug reaction before an autoimmune diagnosis is assigned. The corrective action is to complete the exclusionary workup before starting immunosuppression, because glucocorticoids will obscure the diagnostic yield of subsequent cultures and cytology.

A second error is treating the autoantibody test instead of the patient. A positive antinuclear antibody titre supports a diagnosis of systemic lupus erythematosus but does not by itself mandate treatment. Conversely, a negative titre does not exclude immune-mediated disease when the clinical picture is strong. The test result is one data point in a diagnostic matrix, not the diagnosis.

A third error is failing to recognize that different effector mechanisms require different monitoring. Antibody-mediated cytopenias are tracked by serial blood counts. T cell mediated organ damage, as described in central nervous system autoimmunity, may progress without any change in peripheral blood parameters Autoimmune T cell responses in the central nervous system. For immune-mediated polyarthritis, serial joint evaluation and gait assessment are more informative than acute phase protein measurements.

Limitations of the Evidence

The evidence base for veterinary autoimmunity is uneven. Much of the mechanistic understanding derives from inbred mouse strains such as the NOD mouse, which models type 1 diabetes but does not reproduce the genetic heterogeneity or environmental exposure of clinical veterinary patients The NOD mouse as a model of immune dysregulation. Translating findings from experimental autoimmune encephalomyelitis to spontaneous disease in dogs and cats requires caution, because the induction protocols, the timing of antigen exposure, and the genetic background differ substantially.

Expert opinion still differs on several practical points. The threshold for adding a second immunosuppressive agent, the optimal duration of maintenance therapy, and the value of repeat autoantibody testing during remission all lack controlled data. Some specialists advocate lifelong low-dose maintenance after a single episode of immune-mediated hemolytic anemia, others taper to discontinuation after six to twelve months. Both positions are defensible given the available evidence, and the decision should incorporate the patient's signalment, the severity of the index episode, and the owner's capacity for monitoring.

The role of viral triggers in spontaneous veterinary autoimmunity is similarly unsettled. Experimental data support molecular mimicry, bystander activation, and epitope spreading as mechanisms by which viruses can initiate autoreactivity, but the clinical relevance in companion animals is unclear Viruses and autoimmunity: potential interaction and molecular mechanisms. Documenting a concurrent infection does not prove causation, and withholding immunosuppression because of a positive viral test can be as harmful as ignoring the infection.

Referral, Consultation, and Reporting

Referral to a specialist is warranted when the diagnosis remains uncertain after a complete primary care workup, when the patient fails to respond to first-line therapy, when multiagent immunosuppression is being considered, or when the target organ is the central nervous system, kidney, or bone marrow. Specialist input is also appropriate for immune-mediated polyarthritis that does not respond to glucocorticoids within a defined period, because the differential diagnosis expands to include erosive arthropathies and paraneoplastic syndromes The IL-23-IL-17 axis in inflammatory arthritis.

Laboratory involvement extends beyond diagnostic testing. A clinical pathologist can review blood smears, bone marrow aspirates, and cytology specimens to distinguish immune-mediated destruction from production failure. A veterinary pathologist should evaluate tissue biopsies when the diagnosis rests on histopathology. The Davis-Thompson Foundation maintains educational pathology resources that illustrate the range of autoimmune lesions and their mimics Davis-Thompson Foundation veterinary pathology resources.

Regulatory reporting obligations vary by jurisdiction and production system. In food animals, autoimmune disease is uncommon, but any condition that mimics a notifiable disease must be reported according to local requirements. The World Organization for Animal Health publishes terrestrial animal health standards that define reporting obligations for listed diseases WOAH terrestrial animal health standards. Companion animal practitioners should consult their regional veterinary board for guidance on record keeping and adverse event reporting related to immunosuppressive drug use.

Frequently Asked Questions

How Do I Distinguish Autoimmune Disease from Immune-Mediated Disease When the Target Antigen Is Unknown?

The distinction is practical, not semantic. Autoimmune disease requires demonstrated autoreactivity, such as autoantibodies or self-reactive T cells directed at a defined self-antigen. In many veterinary presentations, the target antigen is never identified, and the diagnosis rests on exclusion of infection, neoplasia, and drug reactions combined with a response to immunosuppressive therapy. The term immune-mediated is therefore more accurate in those cases. Document the evidence level in the record. When autoantibody testing is available, for example Coombs testing in hemolytic anemia, a positive result supports autoimmunity, but a negative result does not exclude it. The MSD Veterinary Manual provides species-specific guidance on which immune-mediated diagnoses are commonly confirmed versus presumptive.

Which Autoimmune Diseases Can Be Confirmed Antemortem, and Which Remain Presumptive?

Antemortem confirmation is achievable when a specific autoantibody assay has validated diagnostic performance. Examples include Coombs-positive immune-mediated hemolytic anemia, acetylcholine receptor antibody testing for myasthenia gravis, and antinuclear antibody testing in systemic lupus erythematosus. Many other conditions, including immune-mediated polyarthritis and inflammatory bowel disease, rely on cytology, histopathology, and exclusion of differentials. Tissue biopsy can support the diagnosis by showing lymphocyte or plasma cell infiltration, but it does not prove autoreactivity. The Davis-Thompson Foundation pathology resources illustrate the histologic patterns that support immune-mediated diagnoses. Communicate the confidence level to the owner and in the record, and revisit the diagnosis if the clinical course diverges from expectations.

How Should I Proceed When Advanced Diagnostic Testing Is Unavailable or Unaffordable?

A structured treatment trial is acceptable when the clinical picture strongly supports immune-mediated disease and infection has been reasonably excluded. Establish objective response criteria before starting therapy, including specific parameters such as packed cell volume, lameness score, or skin lesion area. Reassess at defined intervals and document the response. If the patient fails to improve, reconsider the diagnosis instead of escalating immunosuppression. Regional and production-system constraints may limit access to reference laboratories, and the AVMA practice resources offer guidance on referral and practice standards. A trial of therapy is not a substitute for diagnostic rigor, and the limitations of this approach should be recorded explicitly.

How Does the Diagnostic Approach Change in Food Animals Compared with Companion Animals?

Economic value, herd health context, and regulatory constraints alter the workup. Individual animal diagnostics are often impractical in production settings, and the clinician must weigh the cost of testing against the value of the animal and the risk to the herd. Slaughter surveillance and postmortem examination may be the only feasible diagnostic tools. Withdrawal periods for any treatment must be considered, and current label and formulary references should be consulted before administering immunosuppressive drugs to food animals. The WOAH terrestrial animal health standards address disease surveillance and reporting obligations that may apply when immune-mediated conditions mimic notifiable diseases.

What Should I Document in the Medical Record to Support a Later Review of the Diagnosis?

Record the clinical signs, the differential list, and the specific evidence that excluded infection and neoplasia. Note which autoantibody tests were performed and their results. If a treatment trial was used, document the response criteria, the timeline, and the outcome at each reassessment. Photographs, cytology descriptions, and histopathology reports strengthen the record. When the diagnosis remains presumptive, state that explicitly. The MSD Veterinary Manual emphasizes that immune-mediated diagnoses often require longitudinal follow-up to confirm. A record that supports retrospective review is valuable when the disease relapses, when a second opinion is sought, or when an adverse outcome prompts scrutiny.

How Do I Explain Autoimmune Disease to an Owner Without Overstating Diagnostic Certainty?

Use an analogy that conveys the core mechanism without implying more certainty than exists. Describe the immune system as having lost part of its ability to distinguish self from non-self, and explain that the specific trigger is often unknown. Distinguish between a confirmed diagnosis and a working diagnosis. Explain what tests were done, what they can and cannot show, and why exclusion of infection was important before starting immunosuppression. Be honest about the possibility that the diagnosis may change. The AVMA practice resources provide communication guidance for difficult conversations. Owners need to understand the monitoring plan and the signs of relapse, and they should know that response to treatment is part of the diagnostic picture.

Related Clinical & Scientific Guides

• Hypersensitivity Reactions: Types and Mechanisms
• Therapeutic Decision-Making for Respiratory Infections in Cattle
• Monitoring Fluid Therapy in Critically Ill Veterinary Patients

References and Further Reading

• Cracking the BAFF code.. 2009.
• The NOD mouse: a model of immune dysregulation.. 2005.
• Autoimmune T cell responses in the central nervous system.. 2009.
• Viruses and Autoimmunity: A Review on the Potential Interaction and Molecular Mechanisms.. 2019.
• The IL-23-IL-17 axis in inflammatory arthritis.. 2015.
• The role of antigen presenting cells in multiple sclerosis.. 2011.
• Davis-Thompson Foundation Veterinary Pathology Resources. Davis-Thompson Foundation.
• MSD Veterinary Manual, Professional Edition. MSD Veterinary Manual.
• American Veterinary Medical Association Practice Resources. American Veterinary Medical Association.

Related Articles

• Genetic Diseases in Animals: Mechanisms and Examples
• Therapeutic Decision-Making for Autoimmune Disease in Dogs
• Edema and Shock: Pathophysiologic Mechanisms
• Hypersensitivity Reactions: Types and Mechanisms
• Zoonotic Diseases: Mechanisms and Veterinary Public Health

This article is educational professional reference material for veterinary audiences. It is not a substitute for veterinary diagnosis, individual clinical judgment, current product labeling, or applicable regulatory requirements.