Journal of Immunology and Immunopathology
  • Year: 2013
  • Volume: 15
  • Issue: 1

Role of T Lymphocytes in Regulation of Parasitic Immunity

  • Author:
  • N Kumar, GS Manohar, SP Joshi, R Kumar
  • Total Page Count: 1
  • Page Number: 81 to 81

College of Veterinary and Animal Science, RAJUVAS, Bikaner

Online published on 19 December, 2013.

Abstract

Parasitic protozoa and helminths are a diverse group of organisms which together form a major cause of infectious disease in humans and livestock. Studies in animal models have revealed that T lymphocytes and the cytokines they produce play a crucial role in determining the outcome of parasitic infection in terms of both protective immunity and immunopathology. T cells play important role in both of these events, either directly or by mediating cellular responses or by regulating antibody production. T cells consist of two major subsets, CD4+ (T helper) cells and CD8+ (T cytotoxic) cells. CD4+ cells provide help for antibody production, mediate delayed hypersensitivity responses, and are restricted by class II major histocompatibility factor, while CD8+ cells are associated with cytotoxic or suppressor and recognize antigen in the context of class I antigens. In parasitic infection, both cells may contribute to protection or pathology, although at present the role of CD8+ cells less well understood, possibly because few CD8+ T cell clones directed against parasite antigens have been established. In contrast, the production of T cell lines and clones of CD4+ subset has substantially increased our understanding of these cells in immunologic responses. CD4+ T cells can be divided into two subsets based on the production of type of lymphokines i.e. interleukin- 2 (IL2) and interferon-γ (IFN γ) produced by T helper1 (TH1) cells and IL-4 and IL-5 are produced by TH2 cells. Attributable to different lymphokines produced by these cells, TH1 and TH2 cells have different functions. For example, TH1 cells mediate delayed type hypersensitivity while only TH2 cells can act as helper cells for immunoglobulin-E production.