Journal of Dermatology Research and Skin Care

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +1 (202) 780-3397

Opinion Article - Journal of Dermatology Research and Skin Care (2023) Volume 7, Issue 3

The role of autoimmunity in dermatological diseases.

Bowler Davies*

Department of Dermatology, University of California at San Francisco, USA

*Corresponding Author:
Bowler Davies
Department of Dermatology
University of California
San Francisco, USA

Received:19-May-2023,Manuscript No. AADRSC-23-102550; Editor assigned:23-May-2023, PreQC No. AADRSC-23-102550(PQ); Reviewed:06-Jun-2023, QC No. AADRSC-23-102550; Revised:12-Jun-2023, Manuscript No.AADRSC-23-102550(R); Published:19-Jun-2023, DOI:10.35841/aadrsc- 7.3.151

Citation: Davies B. The role of autoimmunity in dermatological diseases.Dermatol Res Skin Care. 2023; 7(3):151

Visit for more related articles at Journal of Dermatology Research and Skin Care


Dermatological diseases encompass a wide range of conditions that affect the skin, hair, and nails. Many of these diseases have an underlying autoimmune component, where the immune system mistakenly attacks healthy cells and tissues in the skin. This article aims to explore the role of autoimmunity in dermatological diseases, shedding light on the complex connection between immune dysregulation and skin disorders.

Understanding autoimmunity

Autoimmunity occurs when the immune system, which is designed to protect the body from foreign invaders, mistakenly identifies self-antigens as threats and launches an immune response against them. This misguided response leads to tissue damage and inflammation. The mechanisms behind autoimmunity are multifaceted and can involve genetic predispositions, environmental triggers, and dysregulation of immune cells. In dermatological diseases, autoimmunity often manifests as an attack on skin cells, hair follicles, or connective tissues, resulting in a range of clinical manifestations[1].

Autoimmunity in dermatological diseases

Psoriasis is a chronic inflammatory skin disorder characterized by red, scaly patches known as plaques. It is considered an autoimmune disease driven by dysregulation of immune cells and cytokines. T cells, a type of white blood cell, play a central role in psoriasis pathogenesis. In psoriatic lesions, T cells are activated and release inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukins, leading to excessive proliferation of skin cells and inflammation. Genetic factors, such as specific human leukocyte antigen (HLA) variants, contribute to the development of psoriasis, highlighting the autoimmune nature of the disease.

Systemic Lupus Erythematosus (SLE)

SLE is a systemic autoimmune disease that can affect multiple organs, including the skin. Cutaneous lupus erythematosus (CLE) refers to the skin manifestations of SLE. It presents in various forms, such as discoid lupus erythematosus (DLE), subacute cutaneous lupus erythematosus (SCLE), and acute cutaneous lupus erythematosus (ACLE). In SLE, autoantibodies are produced against various self-antigens, including DNA, histones, and Ro/SSA and La/SSB antigens. These autoantibodies can deposit in the skin, leading to inflammation and tissue damage. Additionally, immune complex deposition and complement activation contribute to the development of skin lesions in SLE[2].

Bullous pemphigoid

Bullous pemphigoid is a blistering autoimmune disorder characterized by the presence of subepidermal blisters. It occurs when autoantibodies, specifically IgG antibodies, target and bind to proteins within the basement membrane zone, such as BP180 and BP230. This immune reaction triggers an inflammatory response, attracting immune cells, and leading to the formation of blisters. The exact mechanisms triggering the production of autoantibodies in bullous pemphigoid are still under investigation, but both genetic and environmental factors are believed to contribute to the development of the disease[3].


Dermatomyositis is an inflammatory myopathy characterized by muscle weakness and distinctive skin rashes. It is considered an autoimmune disease involving both the skin and muscles. In dermatomyositis, immune cells infiltrate the blood vessels of the skin, leading to inflammation and damage. Autoantibodies, such as anti-Mi-2, anti-Jo-1, and anti-MDA5 antibodies, are commonly detected in dermatomyositis patients. The exact trigger for the immune response in dermatomyositis remains unclear, but viral infections and genetic factors have been suggested as potential contributors.


Pemphigus encompasses a group of autoimmune blistering diseases characterized by the presence of intraepidermal blisters. The most common types are pemphigus vulgaris (PV) and pemphigus foliaceus (PF). In pemphigus, autoantibodies, mainly IgG antibodies, target and bind to desmogleins, which are proteins responsible for maintaining adhesion between skin cells. This disrupts the cell-cell adhesion, leading to the formation of blisters. Genetic predisposition and environmental triggers, such as medications and infections, can contribute to the development of pemphigus[4].

Treatment approaches

The management of autoimmune dermatological diseases focuses on controlling inflammation, suppressing the immune response, and minimizing tissue damage. Treatment options may include topical or systemic corticosteroids, immunosuppressive agents, biologic therapies, and phototherapy. Topical corticosteroids are commonly used to reduce inflammation and relieve symptoms in localized skin lesions. Systemic corticosteroids or immunosuppressive agents may be prescribed for more severe or widespread disease manifestations. Biologic therapies, such as TNF-alpha inhibitors or monoclonal antibodies targeting specific immune cells or cytokines, have revolutionized the treatment of autoimmune dermatological diseases, providing more targeted and effective approaches.

Future perspectives

Advances in understanding the role of autoimmunity in dermatological diseases have opened doors for innovative treatment approaches. Targeting specific immune cells, cytokines, or signaling pathways involved in autoimmune processes holds promise for developing more effective and tailored therapies. Furthermore, research into personalized medicine, genetic profiling, and the identification of specific autoantibodies may allow for individualized treatment strategies based on patients' specific immune profiles[5].


Autoimmunity plays a significant role in the pathogenesis of various dermatological diseases. The complex interplay between dysregulated immune responses and skin tissues contributes to the clinical manifestations observed in these conditions. Understanding the underlying autoimmune mechanisms is crucial for developing targeted therapeutic interventions that can effectively manage these diseases and improve patients' quality of life. Continued research in the field of autoimmunity and dermatology will likely lead to further breakthroughs, enhancing our understanding and treatment options for autoimmune skin disorders.


  1. Moyle M, Cevikbas F, Harden JL, et al.Understanding the immune landscape in atopic dermatitis: The era of biologics and emerging therapeutic approaches.Exper Dermatol. 2019;28(7):756-68.
  2. Indexed at, Google Scholar, Cross Ref

  3. Simpson EL, Bieber T, Guttman-Yassky E, et al.Two phase 3 trials of dupilumab versus placebo in atopic dermatitis.N Eng J Med. 2016;375(24):2335-48
  4. Indexed at, Google Scholar, Cross Ref

  5. Damsky W, King BA.JAK inhibitors in dermatology: The promise of a new drug class.J Am Acd Dermatol. 2017;76(4):736-44.
  6. Indexed at, Google Scholar, Cross Ref

  7. Wang EH, Sallee BN, Tejeda CI, et al.JAK inhibitors for treatment of alopecia areata.J Invest Dermatol. 2018;138(9):1911-6.
  8. Indexed at, Google Scholar, Cross Ref

  9. Nakatsuji T, Gallo RL.The role of the skin microbiome in atopic dermatitis.Ann Allergy Asthma Immunol. 2019;122(3):263-9.
  10. Indexed at, Google Scholar, Cross Ref

Get the App