PMID- 11399508
OWN - NLM
STAT- MEDLINE
DCOM- 20010906
LR  - 20061115
IS  - 1148-5493 (Print)
IS  - 1148-5493 (Linking)
VI  - 12
IP  - 2
DP  - 2001 Apr-Jun
TI  - Regulation of helper T cell responses to staphylococcal superantigens.
PG  - 210-22
AB  - Staphylococcal superantigens (sAgs) including toxic shock syndrome toxin-1 
      (TSST-1) and related enterotoxins are exoproteins with unique immunobiological 
      properties. They bind to major histocompatibility complex (MHC) class II 
      molecules of antigen-presenting cells outside the peptide groove, and induce 
      massive proliferation of T cells bearing specific V beta determinants. This 
      tri-molecular interaction leads to uncontrolled release of various 
      proinflammatory cytokines especially interferon-gamma (IFN-gamma) and tumor 
      necrosis factor-a (TNF-alpha), the key cytokines causing sAg-mediated shock. The 
      effector T cells involved in this hyper-immune response are predominantly of the 
      T helper-1 (Th1) phenotype. There is also some evidence that polarization to a 
      Th2 response with the production of classical anti-inflammatory cytokines (such 
      as interleukins IL-4 and IL-6) also occurs. Moreover, the emergence of a novel 
      regulatory T cell (Tr1) subset, producing mainly IL-10 but little or no IL-2 and 
      IL-4, has recently been described following repeated sAg stimulation. In this 
      review, the current knowledge regarding the regulation of T helper cell subsets 
      in response to staphylococcal sAgs is critically evaluated, and the role of 
      various cytokines which directly influence T cell differentiation and 
      polarization is summarized. Particular emphasis is directed towards 
      pro-inflammatory as well as anti-inflammatory and regulatory effector functions 
      during toxic shock. Based on this review, we propose that a delayed production of 
      IL-10 by Tr1 cells may be the most prominent driving force in the down-regulation 
      of the Th1 hyper-immune response, and the critical determinant for the eventual 
      recovery of the host.
FAU - Cameron, S B
AU  - Cameron SB
AD  - Division of Infectious Diseases, Department of Medicine, University of British 
      Columbia, Vancouver Hospital, Vancouver, B.C., Canada.
FAU - Nawijn, M C
AU  - Nawijn MC
FAU - Kum, W W
AU  - Kum WW
FAU - Savelkoul, H F
AU  - Savelkoul HF
FAU - Chow, A W
AU  - Chow AW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - France
TA  - Eur Cytokine Netw
JT  - European cytokine network
JID - 9100879
RN  - 0 (Cytokines)
RN  - 0 (Superantigens)
SB  - IM
MH  - Cytokines/immunology
MH  - Humans
MH  - Lymphocyte Activation
MH  - Shock, Septic/epidemiology/immunology/pathology
MH  - Staphylococcus/*immunology
MH  - Superantigens/*immunology
MH  - T-Lymphocytes, Helper-Inducer/*immunology
RF  - 136
EDAT- 2001/06/12 10:00
MHDA- 2001/09/08 10:01
CRDT- 2001/06/12 10:00
PHST- 2001/06/12 10:00 [pubmed]
PHST- 2001/09/08 10:01 [medline]
PHST- 2001/06/12 10:00 [entrez]
PST - ppublish
SO  - Eur Cytokine Netw. 2001 Apr-Jun;12(2):210-22.