T Cells

Abstract

Traditionally, T cells were CD4 1 helper or CD8 1 cytotoxic T cells, and with antibodies, they were the soldiers of immunity. Now, many functionally distinct subsets of activated CD4 1 and CD8 1 T cells have been described, each with distinct cytokine and transcription factor expression. For CD4 1 T cells, these include Th1 cells expressing the transcription factor T-bet and cytokines IL-2, IFN-g, and TNF-b; Th2 cells expressing GATA-3 and the cytokines IL-4, IL-5, and IL-13; and Th17 cells expressing RORgt and cytokines IL-17A, IL-17F, IL-21, and IL-22. The cytokines produced determine the immune inflammation that they mediate. T cells of the effector lineage can be naïve T cells, recently activated T cells, or memory T cells that can be distinguished by cell surface markers. T regulatory cells or spies were characterized as CD8 1 T cells expressing I-J in the 1970s. In the 1980s, suppressor cells fell into disrepute when the gene for I-J was not present in the mouse MHC I region. At that time, a CD4 1 T cell expressing CD25, the IL-2 receptor-a, was identified to transfer transplant tolerance. This was the same phenotype of activated CD4 1 CD25 1 T cells that mediated rejection. Thus, the cells that could induce tolerance and undermine rejection had similar badges and uniforms as the cells effecting rejection. Later, FOXP3, a transcription factor that confers suppressor function, was described and distinguishes T regulatory cells from effector T cells. Many subtypes of T regulatory cells can be characterized by different expressions of cytokines and receptors for cytokines or chemokines. In intense immune inflammation, T regulatory cells express cytokines characteristic of effector cells; for example, Th1-like T regulatory cells express T-bet, and IFN-g-like Th1 cells and effector T cells can change sides by converting to T regulatory cells. Effector T cells and T regulatory cells use similar molecules to be activated and mediate their function, and thus, it can be very difficult to distinguish soldiers from spies.

Chloroquine Autophagic Inhibition Rebalances Th17/Treg-Mediated Immunity and Ameliorates Systemic Lupus Erythematosus

“…Our findings indicated that Th17/Treg immune responses were indeed imbalanced in such patients, corresponding to data from human [6,28] and experimental models [7] previously reported by other researchers. However, the driving force of Th17/Treg imbalance remains unclear [29].…”

Regulation of indoleamine 2,3 dioxygenase and its role in a porcine model of acute kidney allograft rejection

“…TNF-α stimulates IDO independent of IFN-γ 26. In this regard, kidney from Allos showed significant increases in the transcription and translation of the IL-β gene when compared with Autos (figure 4A,B).…”

“…Rejection is associated with activation of antigen presenting cells, which stimulate CD4 + lymphocytes, promoting the release of inflammatory cytokines that include IL-1β, TNF-α and IFN-γ, all of which further activate antigen presenting cells and amplify T cell responses 26. TNF-α stimulates IDO independent of IFN-γ 26.…”

Regulatory T cells and minimal change nephropathy: in the midst of a complex network

“…T regs in the middle of innate and adaptive immunity T regs may play a role in MCN based on their plasticity and multi-functional effects [61]. Basically, these cells are connected to innate immunity by means of CD80 and may, in turn, modulate the levels of pro-and anti-inflammatory compounds.…”