Pemphigus Foliaceus Dog: Comprehensive Veterinary Reference Guide

Pemphigus foliaceus (PF) is the most common autoimmune skin disease in dogs and cats, characterized by the production of autoantibodies against desmosomal adhesion proteins. This results in acantholysis (loss of keratinocyte adhesion) and the formation of pustules, crusts, and erosions primarily affecting the skin. While PF is rarely life-threatening, it can significantly impair quality of life if left untreated or poorly managed.

This comprehensive veterinary reference guide covers the pathogenesis, clinical presentation, diagnostic approach, treatment options including novel therapies like oclacitinib and Bruton's tyrosine kinase inhibitors, and long-term prognosis for pemphigus foliaceus in dogs and cats. It is intended for veterinary professionals, veterinary students, and dedicated pet owners seeking in-depth knowledge.

Quick Q&A

Question: What is the first-line treatment for pemphigus foliaceus in dogs? Answer: The mainstay of therapy is immunosuppression, typically starting with oral glucocorticoids (prednisolone or prednisone) at 1-2 mg/kg twice daily. Adjunctive therapy with oclacitinib, azathioprine, mycophenolate mofetil, or ciclosporin is often added for a steroid-sparing effect. Recent evidence supports oclacitinib as an effective alternative to azathioprine with fewer adverse effects [14].

Introduction

Pemphigus foliaceus (PF) is an autoimmune blistering disease of the skin. It is the most frequently diagnosed pemphigus variant in both dogs and cats, and it also occurs in horses, goats, and occasionally humans. The disease results from the immune system mistakenly targeting desmoglein-1 (Dsg1) and desmocollin-1 (Dsc1), which are cadherin-type adhesion molecules found in the superficial layers of the epidermis [6, 8]. The destruction of these proteins leads to acantholysis: the separation of keratinocytes from one another, forming clefts and pustules within the stratum granulosum and stratum corneum.

PF is considered a "superficial" pemphigus variant, as opposed to pemphigus vulgaris (PV), which targets deeper desmoglein-3 and causes severe oral and mucocutaneous ulceration [17, 32]. In dogs, PF typically spares the oral cavity and mucocutaneous junctions, though exceptions occur.

The disease has a median age of onset around 4-7 years, with certain breeds predisposed, including Akitas, Chow Chows, Bearded Collies, Newfoundlands, Schipperkes, Doberman Pinschers, and English Springer Spaniels. In cats, no strong breed predilection is confirmed, though some reports suggest a higher incidence in middle-aged domestic shorthairs.

Pathogenesis

Autoantibody Targets

The primary autoantigens in canine PF are desmoglein-1 (Dsg1) and desmocollin-1 (Dsc1). Historically, Dsg1 was considered the dominant target, but recent research has re-evaluated the role of anti-Dsc1 IgA autoantibodies. Jordan et al. (2024) demonstrated that anti-Dsc1 IgA autoantibodies are present in a significant subset of canine PF cases, suggesting a more complex humoral immune response than previously appreciated [8]. This finding has implications for diagnosis and potentially for targeted therapy.

In feline PF, circulating anti-keratinocyte autoantibodies are detectable, though the specific target antigens are less well characterized. Levy et al. (2020) confirmed the presence of circulating autoantibodies in feline PF using indirect immunofluorescence, supporting an autoimmune pathogenesis similar to the canine disease [35].

Genetic and Environmental Triggers

The exact trigger for autoantibody production remains unknown, but both genetic and environmental factors are implicated. Drug-induced PF is well recognized, with reports linking the condition to various medications. A recent case report described a putative pemphigus-like reaction to oral fluralaner in a dog, expanding the list of potential drug triggers [11]. Other reported triggers include topical insecticides (metaflumizone, fipronil), antibiotics (sulfonamides), and chronic allergen exposure. In some cases, PF appears to be triggered or exacerbated by chronic skin infections or neoplasia.

Inflammatory Pathways

Microarray gene expression analysis of lesional skin in canine PF has revealed upregulation of immune activation pathways, including B cell signatures, Th1/Th17 pathways, and innate immune responses [10, 27]. Starr et al. (2023) characterized the serum and skin inflammatory profile using multiplex assays, identifying elevated levels of IL-6, IL-8, MCP-1, and other pro-inflammatory cytokines [15]. These findings highlight the complex interplay between humoral and cellular immunity in PF pathogenesis.

A novel area of research involves the role of Bruton's tyrosine kinase (BTK), a key enzyme in B cell receptor signaling. BTK inhibitors, such as rilzabrutinib (PRN1008) and PRN473, have shown promise in both experimental models and clinical trials for canine PF [23, 31, 34, 38]. These agents block B cell activation and autoantibody production, offering a targeted therapeutic approach.

Clinical Presentation

Classic Facial Form

The most common presentation of canine PF is the "classic facial form," characterized by pustules, crusts, and erosions on the nasal planum, periocular skin, pinnae, and ears. Lesions often begin on the face and then spread to the trunk and limbs. The pustules are typically large, fragile, and easily ruptured, leaving behind circular erosions with collarettes of scale. In chronic cases, hyperpigmentation and lichenification may develop.

Trunk-Dominant Form

A distinct "trunk-dominant" variant has been described, in which lesions are concentrated on the ventral abdomen, axillae, and groin, with relative sparing of the face [16, 20]. This form may be more common in certain breeds and may be associated with different autoantibody profiles. Bizikova et al. (2022) found that trunk-dominant PF is associated with anti-Dsc1 autoantibodies, while classic facial PF is more strongly linked to anti-Dsg1 autoantibodies [20]. This distinction has diagnostic and prognostic implications.

Vasculopathic Lesions

Some dogs with PF develop vasculopathic lesions, including purpura, necrosis, and ulceration, particularly on the ear margins, tail tip, and footpads. Zhou et al. (2021) evaluated 41 dogs with PF and found that those with vasculopathic lesions had a more severe clinical course and required more aggressive therapy [30]. The presence of vasculopathy may indicate a more complex immune-mediated process.

Feline Pemphigus Foliaceus

In cats, PF presents differently than in dogs. The most common lesions are crusts and erosions on the face (especially the periocular area, ears, and chin), the nipples, and the claw beds (paronychia). Pustules are less frequently observed due to the thinness of feline skin and the tendency for rapid rupture. Lesions on the footpads and nail beds are particularly characteristic and may be the presenting complaint. Systemic signs such as fever, lethargy, and anorexia are more common in cats than in dogs.

Differential Diagnosis

PF must be differentiated from other pustular and crusting dermatoses. The primary differentials include:

• Superficial pyoderma (bacterial folliculitis): Can be difficult to distinguish clinically. Cytology and response to antibiotics are key. Spriggs et al. (2024) compared cytomorphological features of canine PF and superficial pyoderma, finding that acantholytic keratinocytes are more numerous and more cohesive in PF [7].
• Dermatophytosis: Fungal culture or PCR is necessary.
• Demodicosis: Deep skin scrapings are diagnostic.
• Cutaneous drug reaction: History of recent medication administration.
• Discoid lupus erythematosus (DLE): Typically affects the nasal planum with depigmentation and ulceration. Can occur concurrently with PF (cutaneous polyautoimmunity) [37].
• Pemphigus vulgaris: Deeper ulcers, oral involvement, positive Nikolsky sign [17, 32].
• Sterile neutrophilic dermatosis (Sweet's syndrome): Rare, associated with systemic inflammation [22].

Diagnosis

Cytology

The first step in diagnosis is cytological examination of intact pustules or the underside of crusts. In PF, cytology reveals large numbers of acantholytic keratinocytes (rounded, nucleated keratinocytes with basophilic cytoplasm) and neutrophils, with few or no bacteria. The presence of "rafts" of acantholytic cells is highly suggestive of PF. Eosinophils may also be present, particularly in cats.

Histopathology

A definitive diagnosis of PF requires histopathological examination of skin biopsy samples. Ideally, biopsies should be taken from early, intact pustules. If intact pustules are not available, samples from the edge of erosions or from crusted lesions may be diagnostic, though interpretation can be more challenging.

Histopathological features of PF include:

• Subcorneal or intragranular pustular dermatitis with acantholysis
• Neutrophilic or eosinophilic pustules
• Acantholytic keratinocytes within pustules
• Spongiosis and exocytosis of inflammatory cells
• Variable dermal inflammation

Gedon et al. (2023) compared the histopathological features of trunk-dominant PF with classic facial and insecticide-triggered forms, finding that trunk-dominant cases often show more pronounced follicular involvement and a less prominent neutrophilic component [16].

Immunofluorescence and Immunohistochemistry

Direct immunofluorescence (DIF) testing of skin biopsies can demonstrate deposition of IgG and/or IgA in the intercellular spaces of the epidermis, confirming the autoimmune nature of the disease. Indirect immunofluorescence (IIF) on serum samples can detect circulating autoantibodies, though this test is less commonly used in clinical practice. Levy et al. (2020) validated IIF for feline PF, showing good sensitivity and specificity [35].

Advanced Diagnostics

Enzyme-linked immunosorbent assays (ELISAs) for anti-Dsg1 and anti-Dsc1 autoantibodies are available at specialized laboratories and can aid in diagnosis and monitoring. However, these tests are not yet widely commercialized.

Biomarkers

Emerging research has identified potential biomarkers for PF. Kannan et al. (2024) evaluated biomarkers in canine cytotoxic interface dermatitis reactions, finding similarities and differences that may help distinguish PF from other immune-mediated skin diseases [5]. Starr et al. (2024) identified specific gene expression signatures in lesional skin that could serve as diagnostic or prognostic markers [10].

Treatment

The goal of treatment is to suppress the aberrant immune response, control clinical signs, and maintain remission with minimal adverse effects. Treatment is typically lifelong, though some dogs may achieve long-term remission and require only intermittent therapy.

Glucocorticoids

Systemic glucocorticoids (prednisone or prednisolone at 1-2 mg/kg twice daily) remain the cornerstone of induction therapy. Higher doses (2-4 mg/kg/day) may be needed for severe cases. Once clinical remission is achieved (typically within 2-4 weeks), the dose is gradually tapered over 2-4 months to the lowest effective maintenance dose. In dogs, dexamethasone or triamcinolone may be used if prednisolone is ineffective.

Swales et al. (2019) investigated whether low doses of oral glucocorticoids could be as effective as high doses as the sole treatment for canine PF. Their findings suggested that lower doses (0.5-1 mg/kg/day) may be sufficient for some dogs, but higher doses are still recommended for initial disease control [39].

Steroid-Sparing Agents

Due to the adverse effects of long-term glucocorticoid therapy, most dogs require adjunctive immunosuppressant therapy. The choice of agent depends on the individual patient, concurrent diseases, and owner compliance.

Oclacitinib (Apoquel)

Oclacitinib, a Janus kinase (JAK) inhibitor, has emerged as a promising treatment for canine PF. Originally developed for atopic dermatitis, oclacitinib inhibits JAK1 and JAK3, reducing the production of pro-inflammatory cytokines and the activation of T cells and other immune cells.

Hernandez-Bures et al. (2023) conducted a retrospective analysis comparing oclacitinib to azathioprine in the management of canine PF. The study found that oclacitinib was as effective as azathioprine for induction and maintenance of remission, with a significantly lower incidence of adverse effects [14]. Scranton et al. (2026) reported similar findings in a retrospective analysis of 21 cases of canine PF, pemphigus vulgaris, and mucous membrane pemphigoid treated with oclacitinib [2].

A case report by da Silva et al. (2025) described successful treatment of a dog with PF using oclacitinib as monotherapy, with complete resolution of lesions within 8 weeks [4]. These findings suggest that oclacitinib may be a viable first-line or second-line therapy for canine PF, particularly in dogs that cannot tolerate glucocorticoids or other immunosuppressants.

Azathioprine (Imuran)

Azathioprine is a purine analog that inhibits DNA synthesis in rapidly dividing cells, including lymphocytes. It is commonly used as a steroid-sparing agent in dogs. The typical dose is 2 mg/kg once daily or every other day. Azathioprine is not recommended for use in cats due to the risk of severe bone marrow suppression.

Mycophenolate Mofetil (CellCept)

Mycophenolate mofetil (MMF) inhibits inosine monophosphate dehydrogenase, blocking the proliferation of B and T lymphocytes. Putra et al. (2022) evaluated the steroid-sparing effects of oral MMF as an adjunct immunosuppressant for canine PF. The study found that MMF allowed for a significant reduction in glucocorticoid dose and was well tolerated, with gastrointestinal upset being the most common adverse effect [26]. Fukushima et al. (2021) reported similar findings, noting that MMF was effective and safe in dogs with immune-mediated disease [29].

Ciclosporin (Atopica, Cyclavance)

Ciclosporin is a calcineurin inhibitor that suppresses T cell activation. Chong et al. (2022) evaluated the steroid-sparing effect of oral modified ciclosporin for treatment of canine PF. The study found that ciclosporin allowed for a significant reduction in glucocorticoid dose, with good long-term tolerability [21].

Yun et al. (2020) reported a case of concurrent PF and hyperadrenocorticism in a dog successfully managed with a combination of azathioprine, ciclosporin, and ketoconazole, highlighting the need for tailored therapy in complex cases [33].

Chlorambucil (Leukeran)

Chlorambucil is an alkylating agent used as a second-line therapy for refractory PF. It is particularly useful in cats. The typical dose is 0.1-0.2 mg/kg once daily or every other day.

Bruton's Tyrosine Kinase Inhibitors

Bruton's tyrosine kinase (BTK) inhibitors represent a novel, targeted approach to treating autoimmune diseases. BTK is a critical enzyme in B cell receptor signaling, and its inhibition blocks B cell activation and autoantibody production.

Goodale et al. (2020) conducted an open trial of the BTK inhibitor PRN1008 (rilzabrutinib) in the treatment of canine PF. The study found that PRN1008 was effective in reducing clinical signs and was well tolerated [34]. A subsequent study by the same group evaluated PRN473, a topical BTK inhibitor, with similar positive results [38]. Owens et al. (2022) described the discovery and development of PRN473 and PRN1008, highlighting their potential for treating immune-mediated diseases in dogs and humans [23].

Langrish et al. (2021) elucidated the anti-inflammatory mechanisms of rilzabrutinib, demonstrating its ability to inhibit B cell activation, reduce autoantibody production, and suppress inflammatory cytokine release [31]. These agents are not yet commercially available but represent a promising future treatment option.

Therapeutic Plasma Exchange

For severe, generalized, or refractory PF, therapeutic plasma exchange (TPE) may be considered. Edmonds et al. (2024) reported a case of severe, generalized canine PF that responded dramatically to TPE after failing conventional therapy [13]. TPE removes circulating autoantibodies and inflammatory mediators, providing rapid clinical improvement. However, it is expensive, requires specialized equipment, and is only available at referral centers.

Human Intravenous Immunoglobulin (hIVIG)

Human intravenous immunoglobulin (hIVIG) has been used as a rescue therapy for refractory PF. However, its use is limited by cost and the risk of adverse effects, including acute hemolytic anemia, as reported by Koo et al. (2022) [25].

Topical Therapy

Topical therapy is an important adjunct to systemic treatment. Antiseptic shampoos (chlorhexidine, benzoyl peroxide) can help control secondary bacterial infections. Topical glucocorticoids (e.g., hydrocortisone aceponate) may be applied to localized lesions.

Monitoring and Adverse Effects

Regular monitoring is essential for all dogs receiving immunosuppressive therapy. This includes:

• Complete blood count (CBC) and serum biochemistry every 2-4 weeks during induction, then every 3-6 months during maintenance
• Urinalysis to monitor for urinary tract infections
• Blood pressure monitoring for dogs receiving glucocorticoids
• Monitoring for signs of infection, gastrointestinal upset, pancreatitis, and bone marrow suppression

Prognosis

The prognosis for PF is generally good with appropriate treatment. Most dogs achieve remission within 4-8 weeks of initiating therapy, and many can be maintained on low-dose or every-other-day therapy. However, PF is a chronic disease that typically requires lifelong management.

Factors associated with a poorer prognosis include:

• Severe or generalized disease at presentation
• Presence of vasculopathic lesions [30]
• Concurrent diseases (e.g., hyperadrenocorticism, diabetes mellitus)
• Poor owner compliance
• Adverse effects of therapy

Zhou et al. (2021) found that dogs with PF and vasculopathic lesions had a more severe clinical course and required more aggressive therapy, but the overall prognosis remained favorable with appropriate management [30].

In cats, the prognosis is also good, though some cats may be more difficult to manage due to adverse effects of therapy and the need for long-term medication.

Prevention

There is no known way to prevent PF, as the underlying cause is autoimmune. However, certain measures may reduce the risk of flares:

• Avoid known drug triggers (e.g., fluralaner, topical insecticides) [11]
• Manage concurrent allergies and skin infections promptly
• Maintain a healthy weight and diet to support the immune system
• Regular veterinary check-ups to monitor for early signs of disease

Special Considerations

Pemphigus Foliaceus in Cats

Feline PF presents unique challenges. Cats are more prone to adverse effects from glucocorticoids, including diabetes mellitus, pancreatitis, and immunosuppression. Lower starting doses of prednisolone (1-2 mg/kg once daily) are often used, and steroid-sparing agents such as chlorambucil are preferred. Oclacitinib has been used in cats, though data are limited. Wehber et al. (2026) reported the clinical efficacy and adverse events of oclacitinib administration for skin disease in 238 cats, providing valuable safety data [1].

Concurrent Autoimmune Disease

PF can occur concurrently with other autoimmune diseases, a phenomenon known as cutaneous polyautoimmunity. Levy et al. (2020) reported two unrelated dogs with concurrent PF and generalized discoid lupus erythematosus (GDLE) [37]. This highlights the need for thorough diagnostic evaluation in dogs with atypical clinical presentations.

Drug-Induced PF

Drug-induced PF is well recognized and should be suspected in dogs that develop PF within 2-4 weeks of starting a new medication. Common triggers include topical insecticides (metaflumizone, fipronil), antibiotics (sulfonamides), and, as recently reported, oral fluralaner [11]. Withdrawal of the offending drug may lead to resolution of clinical signs, though some dogs require immunosuppressive therapy.

PF and Neoplasia

PF has been associated with underlying neoplasia, particularly lymphoma. Suárez-Bonnet et al. (2019) reported a case of concurrent pemphigus erythematosus and cutaneous epitheliotropic lymphoma in a Labrador Retriever [40]. This association, known as paraneoplastic pemphigus, is rare but should be considered in older dogs with atypical presentations.

Emerging Therapies and Research

Gene Expression Analysis

Microarray gene expression analysis has identified specific gene signatures in lesional skin of dogs with PF. Starr et al. (2024) found upregulation of genes involved in B cell activation, immune signaling, and keratinocyte differentiation [10]. Raef et al. (2021) identified B cell signatures and immune activation pathways similar to human disease [27]. These findings may lead to the development of targeted therapies.

Biomarkers for Canine Atopic Dermatitis

While not directly related to PF, research on biomarkers for canine atopic dermatitis (CAD) may have implications for PF. Kaur et al. (2024) identified PDE4D and miR-203 as promising biomarkers for CAD [9]. Similar approaches could be applied to PF to improve diagnosis and monitoring.

Bruton's Tyrosine Kinase Inhibitors

As discussed above, BTK inhibitors represent a promising new class of drugs for PF. Clinical trials are ongoing, and these agents may become commercially available in the coming years.

Oclacitinib in Cats

The use of oclacitinib in cats is an area of active research. Wehber et al. (2026) reported that oclacitinib was effective and well tolerated in cats with various skin diseases, though data on PF specifically are limited [1]. Further studies are needed to establish the safety and efficacy of oclacitinib in feline PF.

Regional Considerations

North America

In the United States and Canada, PF is the most common autoimmune skin disease in dogs. The availability of advanced diagnostics (e.g., DIF, IIF) and therapies (e.g., oclacitinib, ciclosporin) is excellent. The AAHA and AVMA provide guidelines for the management of immune-mediated diseases.

Europe

In Europe, the EMA regulates veterinary medicines. Oclacitinib is approved for use in dogs for atopic dermatitis and is used off-label for PF. Ciclosporin is widely available. The FVE provides guidance on the use of immunosuppressive agents.

Australia

In Australia, the AVA and DAFF regulate veterinary medicines. Oclacitinib is available for use in dogs. The availability of advanced diagnostics may be more limited in rural areas.

United Kingdom

In the UK, the Veterinary Medicines Directorate (VMD) regulates medicines. Oclacitinib and ciclosporin are approved for use in dogs. The BSAVA provides guidelines for the management of autoimmune skin disease.

Conclusion

Pemphigus foliaceus is a challenging but manageable autoimmune skin disease in dogs and cats. Early diagnosis, appropriate immunosuppressive therapy, and careful monitoring are essential for achieving and maintaining remission. The availability of novel therapies such as oclacitinib and BTK inhibitors has expanded the treatment options and improved the prognosis for affected animals.

Veterinarians should maintain a high index of suspicion for PF in dogs and cats with pustular or crusting dermatoses, particularly those affecting the face, ears, and footpads. Definitive diagnosis requires cytology and histopathology, and treatment should be tailored to the individual patient.

With appropriate management, most dogs and cats with PF can enjoy a good quality of life. Ongoing research into the pathogenesis and treatment of PF holds promise for even better outcomes in the future.

References

1. Wehber MR, Eisenschenk MC, Young AJ, et al. A Retrospective Case Series Reporting the Clinical Efficacy and Adverse Events of Oclacitinib Administration for Skin Disease in 238 Cats. Vet Dermatol. 2026. [1]

2. Scranton BL, Tomich LM, Lam ATH, et al. Treatment of Canine Pemphigus Foliaceus, Pemphigus Vulgaris and Mucous Membrane Pemphigoid With Oclacitinib: A Retrospective Analysis of 21 Cases. Vet Dermatol. 2026. [2]

3. van den Berg J, Lange K. [Pemphigus vulgaris - a case report]. Tierarztl Prax Ausg K Kleintiere Heimtiere. 2025. [3]

4. da Silva MMC, Bernardini M, Lopes NL. Use of Oclacitinib in the treatment of pemphigus foliaceus in a dog: case report. Braz J Vet Med. 2025. [4]

5. Kannan S, Wong NB, Ryan GE, et al. Evaluating biomarkers in canine cytotoxic interface dermatitis reactions to account for clinical and histopathological similarities and differences. Front Vet Sci. 2024. [5]

6. Jordan TJM, Bizikova P. Canine and Feline Pemphigus Foliaceus-an Update on Pathogenesis and Treatment. Vet Clin North Am Small Anim Pract. 2025. [6]

7. Spriggs TS, Gedon NKY, Linder KE, et al. Comparison of selected cytomorphological features of canine pemphigus foliaceus and superficial pyoderma. Vet Dermatol. 2024. [7]

8. Jordan TJM, Mamo LB, Olivry T, et al. Re-evaluating the prevalence of anti-desmocollin-1 IgA autoantibodies in canine pemphigus foliaceus. Vet Immunol Immunopathol. 2024. [8]

9. Kaur G, Xie C, Dong C, et al. PDE4D and miR-203 are promising biomarkers for canine atopic dermatitis. Mol Biol Rep. 2024. [9]

10. Starr H, Howerth EW, Leon R, et al. Microarray Gene Expression Analysis of Lesional Skin in Canine Pemphigus Foliaceus. Vet Sci. 2024. [10]

11. Dalmau A, Ordeix L. Putative pemphigus-like reaction to oral fluralaner in a dog. Vet Dermatol. 2024. [11]

12. Kwak JH, Na CH, Shin BS, et al. Pyoderma gangrenosum developed from aggravated pemphigus foliaceous after dog bite. Dermatol Reports. 2023. [12]

13. Edmonds KB, Her J, Langston C, et al. Efficacy of therapeutic plasma exchange in a case of severe, generalised canine pemphigus foliaceus. Vet Dermatol. 2024. [13]

14. Hernandez-Bures A, Bidot WA, Griffin CE, et al. The use of oclacitinib compared to azathioprine in the management of canine pemphigus foliaceus: A retrospective analysis. Vet Dermatol. 2023. [14]

15. Starr H, Howerth E, Gogal R Jr, et al. Characterization of the serum and skin inflammatory profile in canine pemphigus foliaceus using multiplex assay and quantitative real-time polymerase chain reaction (qRT-PCR). Vet Immunol Immunopathol. 2023. [15]

16. Gedon NKY, Bizikova P, Olivry T, et al. Histopathological characterisation of trunk-dominant canine pemphigus foliaceus, and comparison with classic facial and insecticide-triggered forms. Vet Dermatol. 2023. [16]

17. Bizikova P, Linder KE, Anderson JG. Erosive and ulcerative stomatitis in dogs and cats: which immune-mediated diseases to consider? J Am Vet Med Assoc. 2023. [17]

18. Bizikova P, Olivry T, Linder K, et al. Spontaneous autoimmune subepidermal blistering diseases in animals: a comprehensive review. BMC Vet Res. 2023. [18]

19. Kim S, Kim Y, Kim HJ. Case report: Uncommon immune-mediated skin disease involving systemic disorders in dogs. Front Vet Sci. 2022. [19]

20. Bizikova P, Linder KE, Mamo LB. Trunk-dominant and classic facial pemphigus foliaceus in dogs - comparison of anti-desmocollin-1 and anti-desmoglein-1 autoantibodies and clinical presentations. Vet Dermatol. 2022. [20]

21. Chong E, Austel M, Banovic F. A Retrospective Evaluation of the Steroid-Sparing Effect of Oral Modified Ciclosporin for Treatment of Canine Pemphigus Foliaceus. Vet Sci. 2022. [21]

22. Cho A, Bae H, Shin S, et al. Sterile Neutrophilic Dermatosis (Sweet's Syndrome) Associated With Systemic Inflammatory Response Syndrome in a Maltese Dog: A Case Report. Front Vet Sci. 2022. [22]

23. Owens TD, Brameld KA, Verner EJ, et al. Discovery of Reversible Covalent Bruton's Tyrosine Kinase Inhibitors PRN473 and PRN1008 (Rilzabrutinib). J Med Chem. 2022. [23]

24. Martinez N, McDonald B, Crowley A. A case report of the beneficial effect of oclacitinib in a dog with pemphigus vulgaris. Vet Dermatol. 2022. [24]

25. Koo Y, Yun T, Chae Y, et al. Suspected human intravenous immunoglobulin-induced acute haemolytic anaemia in a dog. J Small Anim Pract. 2022. [25]

26. Putra A, Austel M, Banovic F. A retrospective evaluation of the steroid sparing effects of oral mycophenolate mofetil (MMF) as an adjunct immunosuppressant for the treatment of canine pemphigus foliaceus. Vet Dermatol. 2022. [26]

27. Raef HS, Piedra-Mora C, Wong NB, et al. Gene Expression Analysis in Four Dogs With Canine Pemphigus Clinical Subtypes Reveals B Cell Signatures and Immune Activation Pathways Similar to Human Disease. Front Med (Lausanne). 2021. [27]

28. Curtiss JB, Lewis M, Mitchell EP. Pemphigus foliaceus in Arabian oryx (Oryx leucoryx). Vet Pathol. 2021. [28]

29. Fukushima K, Lappin M, Legare M, et al. A retrospective study of adverse effects of mycophenolate mofetil administration to dogs with immune-mediated disease. J Vet Intern Med. 2021. [29]

30. Zhou Z, Corner S, Petersen A, et al. Clinical presentation, treatment and outcome in dogs with pemphigus foliaceus with and without vasculopathic lesions: an evaluation of 41 cases. Vet Dermatol. 2021. [30]

31. Langrish CL, Bradshaw JM, Francesco MR, et al. Preclinical Efficacy and Anti-Inflammatory Mechanisms of Action of the Bruton Tyrosine Kinase Inhibitor Rilzabrutinib for Immune-Mediated Disease. J Immunol. 2021. [31]

32. Tham HL, Linder KE, Olivry T. Deep pemphigus (pemphigus vulgaris, pemphigus vegetans and paraneoplastic pemphigus) in dogs, cats and horses: a comprehensive review. BMC Vet Res. 2020. [32]

33. Yun T, Koo Y, Kim S, et al. Combination therapy with azathioprine, cyclosporine and ketoconazole in a dog with concurrent pemphigus foliaceus and hyperadrenocorticism - Case report. Acta Vet Hung. 2020. [33]

34. Goodale EC, White SD, Bizikova P, et al. Open trial of Bruton's tyrosine kinase inhibitor (PRN1008) in the treatment of canine pemphigus foliaceus. Vet Dermatol. 2020. [34]

35. Levy BJ, Mamo LB, Bizikova P. Detection of circulating anti-keratinocyte autoantibodies in feline pemphigus foliaceus. Vet Dermatol. 2020. [35]

36. Linek M, Doelle M, Leeb T, et al. ATP2A2 SINE Insertion in an Irish Terrier with Darier Disease and Associated Infundibular Cyst Formation. Genes (Basel). 2020. [36]

37. Levy BJ, Linder KE, Mamo LB, et al. Cutaneous polyautoimmunity in two unrelated dogs: pemphigus foliaceus and generalized discoid lupus erythematosus. Vet Dermatol. 2020. [37]

38. Goodale EC, Varjonen KE, Outerbridge CA, et al. Efficacy of a Bruton's Tyrosine Kinase Inhibitor (PRN-473) in the treatment of canine pemphigus foliaceus. Vet Dermatol. 2020. [38]

39. Swales N, Place E, Barnard N, et al. Are low doses of oral glucocorticoids as effective as high doses as the sole treatment for canine pemphigus foliaceus? Vet Rec. 2019. [39]

40. Suárez-Bonnet A, García-González B, Ramírez GA, et al. Pemphigus erythematosus and cutaneous epitheliotropic lymphoma in a Labrador Retriever dog. Iran J Vet Res. 2019. [40]