T helper cell populations: As flexible as the skin?

Abstract

T helper cells can be defined by the cytokines they produce and are divided into Th1, Th2, Th17, T FH or regulatory T cells. Th17 cells have been shown to produce, in addition to IL-17, IL-22. In the current issue of the European Journal of Immunology, an article by Larsen et al. (Eur. J. Immunol. 2011. 41: 2596-2605 provides evidence that human T helper cells, like murine cells, can also express IL-22 in the absence of the other T helper cell signature cytokines. Moreover, they show that these IL-22-producing cells, namely Th22 cells, can be found in the skin of psoriasis patients, where they might contribute to the pathogenesis of this inflammatory skin disease. Finally, they show that, molecularly, Th22 cells are related to Th17 cells, and might therefore be derived from the latter. In this Commentary, the development of the pro-inflammatory T helper populations in the skin are discussed and a model that explains the development of Th22 cells found in the skin of psoriasis patients is proposed.

To Be 17 Again — Anti–Interleukin-17 Treatment for Psoriasis

“…8 CD4+ T cells extracted from psoriatic skin lesions produce high levels of interleukin-17, 9 but the major source of interleukin-17 seems to be the gamma-delta T cells that invade the skin of patients with psoriasis. 13,14 In line with these findings, interleukin-22 seems to play an important role in imiquimod-induced psoriasis, since the disease can be prevented by administration of antibodies targeting interleukin-22 and does not develop in interleukin-22-deficient mice. 10,11 In addition to interleukin-17, the Th17-related cytokine interleukin-22 is also found in psoriatic lesions.…”

Sex steroid deficiency–associated bone loss is microbiota dependent and prevented by probiotics

“…Th17 cells are an osteoclastogenic population of CD4 + T cells (45,46) defined by the capacity to produce IL-17 (47). Th17 cells potently induce osteoclastogenesis by secreting IL-17A, RANKL, TNF, IL-1, and IL-6, along with low levels of IFNγ (48)(49)(50). IL-17A stimulates the release of RANKL by all osteoblastic cells including osteocytes (42,51) and increases the osteoclastogenic activity of RANKL by upregulating RANK (52).…”

PTH induces bone loss via microbial-dependent expansion of intestinal TNF+ T cells and Th17 cells

“…Th17 cells play a pivotal role in the bone loss resulting from pathologic conditions such as psoriasis, rheumatoid arthritis, periodontal disease, and inflammatory bowel disease 20,41 . In these inflammatory states, Th17 cells potently induce osteoclastogenesis by secreting IL-17A, RANKL, TNF, IL-1, and IL-6, along with low levels of IFNγ [42][43][44] . While Th17 cells contribute to pathologic bone destruction in autoimmune diseases, the bone erosion induced by Th17 cells serves an important protective role in diseases such as periodontitis, which is one of the most common infectious diseases, where Th17 cell-induced tooth loss is critical for eradicating bacteria from infected oral cavities and surfaces 45 .…”