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Special Features of Adaptive Immunity

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The adaptive immune system, a crucial component of the overall immune response, offers a highly specialized defense against pathogens. It involves specific cell types and features, enabling it to combat infections effectively and efficiently.
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Related Experiment Video

Updated: Jun 22, 2026

Examination of Thymic Positive and Negative Selection by Flow Cytometry

Examination of Thymic Positive and Negative Selection by Flow Cytometry

Published on: October 8, 2012

How the immune system achieves self-nonself discrimination during adaptive immunity.

Hong Jiang¹, Leonard Chess

¹Institute of Immunology, School of Medicine, Shanghai Jiaotong University, Shanghai, PR China.

Advances in Immunology

|May 30, 2009

Summary

The Avidity Model explains self-nonself discrimination through T cell receptor (TCR) avidity, not just antigen structure. This model highlights how regulating intermediate-avidity T cells can control autoimmunity while preserving immunity to pathogens.

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Area of Science:

Immunology
Autoimmunity
T cell biology

Background:

Self-nonself discrimination is crucial for immune system function, preventing autoimmunity.
Current models inadequately explain the complexities of immune tolerance and autoimmune disease development.
T cell fate is influenced by interactions with antigen-presenting cells (APCs) in the thymus and periphery.

Purpose of the Study:

To propose the Avidity Model of Self-Nonself Discrimination.
To explain how T cell receptor (TCR) avidity, rather than just antigen structure, dictates immune responses.
To provide a unified framework for understanding immunological disorders and autoimmune diseases.

Main Methods:

Conceptual framework integrating central thymic selection and peripheral immune regulation.
Analysis of T cell survival and fate based on TCR avidity with MHC/antigen peptides on APCs.
Examination of peripheral T cell repertoire composition and its role in self-tolerance.

Main Results:

High-avidity T cell clones recognizing self-antigens are deleted in the thymus, leaving intermediate and low-avidity clones.
Intermediate-avidity self-reactive T cells in the periphery pose a risk for developing autoimmune diseases.
Peripheral downregulation of intermediate-avidity T cells, including self-reactive ones, can control autoimmunity without compromising anti-infection immunity.

Conclusions:

The Avidity Model posits that immune tolerance is achieved by modulating T cell activation avidity.
Peripheral immune regulation, exemplified by Qa-1-restricted CD8(+) T cells, selectively targets intermediate-avidity T cells.
This model offers a novel perspective on autoimmune disease development and control, unifying disparate immunological concepts.