Th cell subsets

Grencis, R.K, Hiiltner, L. and Else, K.J. (1991) Host protective immunity to Trichinella spiralis in mice activation of Th cell subsets and lymphokine... 

Else, KJ., Hultner, L. and Grencis, R.K. (1992) Cellular immune responses to the murine nematode parasite Trichuris muris. II. Differential induction of TH-cell subsets in resistant versus susceptible mice. Immunology 75, 232-237. 

Zubiaga, A.M., Munoz, E. and Huber, B.T. (1992). IL-4 and IL-2 selectively rescue Th cell subsets from glucocorticoid-induced apoptosis. J. Immunol. 149, 107-112. 

Boyaka PN, Ohmura M, Fujihashi K et al. Chimeras of labile toxin one and cholera toxin retain mucosal adjuvanticity and direct Th cell subsets via their B subunit. J Immunol 2003 170(l) 454-462. 

Fig.1. Differentiation ofT cells content of micromilieu and several cytokines and other cofactors released from DCs are essential for the differentiation of naive T cells into T-helper(Th)l,Th2,Th9,Thl7 effectorT-cell subsets. 

In 2006, another subset of Th cells was recognized, known as Thl7 cells [89]. These cells have been described to exert major functions in induction of tissue inflammation and... 

These are supplied by the secretion of peptide molecules (termed cytokines or lymphokines) fiom a subset of the T-cell family (the helper T cells, TH cells). These peptide molecules (interleukins (IL) 2,4,5 and 6) stimulate the B cells to proliferate, undergo clonal expansion and mature into plasma cells which secrete antibody and also into the longer-hving, non-dividing memory cells. 

Eczema does not occur in the absence ofT cells. Here we provide an overview on the regulatory impact which T cells have on the establishment and maintenance of atopic dermatitis. Particularly, we outline the role of different T-helper cell subsets (i.e.Th-l,Th-2,T-regulatory andTh-17 cells) and their distinct influence on the cutaneous inflammatory reaction at different stages of the disease. Eczema is characterized by epidermal inflammation and thus T-cell/ker-atinocyte interactions are of particular relevance in this condition. Alterations in innate and adaptive immunity involving cells result in susceptibility to skin infections and in hyperreactivity reactions to environmental stimuli which in turn determine the course and severity of atopic dermatitis. Copyright 2008 S. Karger AG, Basel... 

Major Histocompatibility Complex Class I and II Expression. INFy is the principal enhancer of MHC class I expression on many different types of cells. In contrast to type IIFN, it is also an inducer of MHC class II expression in AFCs (mast cells included) and lymphocytes, promoting the activation of class Il-restricted CD4 T cells. These cells are an important target for IFNy, leading to the differentiation of the Th 1 subset and inhibiting the proliferation of Th2 cells. 

The Th-1 /Th-2 paradigma forms a core mechanism regulating the nature of an immune response. More recently, this concept was further developed by identifying Th-subsets with predominantly suppressing properties, T-regulatory cells (Treg). These cells also play a major role in keeping those cells at rest, which have escaped central tolerance (peripheral self tolerance). 

It is clear that the type 2 cytokines IL-4, IL-9 and IL-13 play an obligatory role in host resistance to nematode infection whereas type 1 responses promote host susceptibility. Therefore, given that susceptibility to nematode infection is not due to a lack of responsiveness perse, but rather the development of an inappropriate response, it is important to understand the factors that influence the induction and expansion of Th subset responses and so control infection outcome. Studies in nematode models and other systems have addressed these questions and identified the importance of host genetic factors, the nature of the antigen and the antigen presenting cell, co-stimulatory molecules on these cells, and the cytokine and chemokine environment immediately following induction of the response. 

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