What is the role of T lymphocytes in the pathophysiology of guttate psoriasis?

Updated: Oct 03, 2019
  • Author: Kirstin Altman, MD; Chief Editor: Dirk M Elston, MD  more...
  • Print
Answer

Answer

Histologic studies of early-stage psoriatic skin lesions reveal that the activation of T lymphocytes, endothelial cells, and macrophages precedes epidermal proliferation. [36] The increased proliferation of the epidermal layer characteristic of psoriasis might be induced by activated T lymphocytes via the production of cytokines. Indeed, group A streptococcal antigen–specific T lymphocytes, which secrete high levels of gamma interferon, can be consistently isolated from guttate psoriatic skin lesions.

Consistent with the role of T lymphocytes is the concept of superantigenic stimulation by certain streptococcal components or products. Examples of superantigens produced by group A beta-hemolytic streptococci are streptococcal pyogenic exotoxins (SPE) types A, B, and C; a 22-kd pepsin fragment of M type-5 protein; S pyogenes– derived cytoplasmic membrane–associated protein (CAP); and secretion-type CAP (SCAP). [37]

In general, unlike a conventional peptide antigen, a superantigen stimulates T cells almost solely through the beta variable (Vβ) portion of the T-cell receptor and induces an expansion of both CD4+ and CD8+ T cells. Therefore, an increased representation of Vβ2+ T lymphocytes, such as that in both the epidermis and the dermis of guttate psoriatic lesions, compared with that of lymphocytes from the peripheral blood of the same patients and lymphocytes in normal skin, strongly suggests that T-cell stimulation by a superantigen is probably involved. [38]

It appears that patients with guttate psoriasis respond to group A streptococcal antigen presentation in the same way as nonpsoriatic patients. However, the magnitude of their response is much greater. [3]

The fungus Malassezia furfur has been associated with the appearance of psoriatic lesions, but a causative role has not been proven. A study by Aydogan et al showed that the prevalence of M furfur was similar in patients with psoriasis and those without. However, in psoriatic patients with M furfur, cytokines important in the regulation of helper T-lymphocytes (Th2 cells), such as IL-4, IL-10, and IL-13, were markedly downregulated as compared to normal controls and psoriatic patients without M furfur. Thus, cytokine dysregulation appears to be important in the development of psoriasis in this patient population. [39]


Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!