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Related Experiment Video

Updated: Jul 10, 2026

Determining Optimal Cytotoxic Activity of Human Her2neu Specific CD8 T cells by Comparing the Cr51 Release Assay to the xCELLigence System

Determining Optimal Cytotoxic Activity of Human Her2neu Specific CD8 T cells by Comparing the Cr51 Release Assay to the xCELLigence System

Published on: August 8, 2012

Infection breaks T-cell tolerance.

M Röcken¹, J F Urban, E M Shevach

¹Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892.

|September 3, 1992

Summary

This summary is machine-generated.

Infection with Nippostrongylus brasiliensis can break T-cell tolerance established by Staphylococcus enterotoxin B (SEB). This suggests infectious agents may trigger autoimmune diseases by activating anergic T cells.

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Area of Science:

Immunology
Autoimmunity
Infectious Disease

Background:

T-cell tolerance, established via clonal deletion or anergy, prevents autoimmune responses.
Autoreactive T cells are normally suppressed to maintain self-tolerance.

Purpose of the Study:

To investigate if concomitant infection can break established T-cell tolerance.
To determine the mechanism by which infectious agents might circumvent T-cell tolerance.

Main Methods:

Induction of T-cell tolerance in mice using Staphylococcus enterotoxin B (SEB).
Challenging tolerant T cells in vitro with SEB to assess cytokine production (interleukin-2, interleukin-4).
Infecting tolerant mice with the nematode Nippostrongylus brasiliensis and analyzing T-cell responses in vivo.

Main Results:

SEB-tolerant T cells did not produce interleukin-2 or -4 upon in vitro SEB challenge.
N. brasiliensis infection in SEB-tolerant mice led to normal expansion of tolerant T cells.
Infection also resulted in increased SEB-reactive, interleukin-4-producing T cells in both tolerant and normal animals.

Conclusions:

Nippostrongylus brasiliensis infection effectively circumvents SEB-induced T-cell tolerance.
Infectious agents may initiate autoimmunity by activating anergic T cells through alternative pathways.
This study highlights a potential mechanism for infectious triggers in the development of autoimmune diseases.