IL-23-dependent IL-17 drives Th1-cell responses followingMycobacterium bovisBCG vaccination

IL-23-dependent IL-17 drives Th1-cell responses following Mycobacterium bovis BCG vaccination.

The generation of effective type 1 T helper (Th1)-cell responses is required for immunity against intracellular bacteria. However, some intracellular bacteria require interleukin (IL)-17 to drive Th1-cell immunity and subsequent protective host immunity. Here, in a model of Mycobacterium bovis Bacille Calmette-Guerin (BCG) vaccination in mice, we demonstrate that the dependence on IL-17 to driv...

IL-23 drives pathogenic IL-17-producing CD8+ T cells.

IL-17-producing CD8(+) T cells (Tc17) appear to play a role in a range of conditions, such as autoimmunity and cancer. Thus far, Tc17 cells have been only marginally studied, resulting in a paucity of data on their biology and function. We demonstrate that Tc17 and Th17 cells share similar developmental characteristics, including the previously unknown promoting effect of IL-21 on Tc17 cell dif...

Cytokines (IL-17, IL-23, and IL-33) in Systemic lupus erythematosus in Trinidad and Tobago.

Systemic lupus erythematosus (SLE) is the most common autoimmune disease. It is characterized by the presence of hundreds of autoantibodies against many organs and tissues, including the presence of a large number of autoantibodies, which are specific to self-antigens mainly of nuclear origin such as Smith antigen, double-stranded DNA (dsDNA), anti-Sjögren’s syndrome-related antigen A and B (SS...

Role of interleukin-23 (IL-23) receptor signaling for IL-17 responses in human Lyme disease.

Interleukin-23 (IL-23) is known to play a crucial role in the development and maintenance of T helper 17 cells. It has been previously demonstrated that IL-17 is involved in experimental Lyme arthritis, caused by Borrelia burgdorferi bacteria. However, the precise role of the IL-23 receptor (IL-23R) for the B. burgdorferi-induced IL-17 responses or human Lyme disease has not yet been elucidated...

Innate IL-12 and IL-23 Production Cell Responses through IL-17 Induction of Th17 Cells Induce Colitis and Promote Th1