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Special Features of Adaptive Immunity

Special Features of Adaptive Immunity

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.
The primary cell types involved in adaptive immunity are T cells and B cells. Each type has a unique role in defending the body against pathogens. T cells are responsible for cell-mediated immunity. They identify and eliminate infected cells directly,...

T Cell Types and Functions

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...

T Cell Activation and Clonal Selection

T Cell Activation and Clonal Selection

T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
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B Cell Activation and Differentiation

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The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...

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Updated: Apr 7, 2026

Generation of Induced Regulatory T Cells from Primary Human Naïve and Memory T Cells

Generation of Induced Regulatory T Cells from Primary Human Naïve and Memory T Cells

Published on: April 16, 2012

mir-181a-1/b-1 Modulates Tolerance through Opposing Activities in Selection and Peripheral T Cell Function.

Steven A Schaffert¹, Christina Loh², Song Wang²

¹Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305; Baxter Laboratory in Stem Cell Biology, Stanford University School of Medicine, Stanford, CA 94305; Program of Immunology, Stanford University School of Medicine, Stanford, CA 94305;

Journal of Immunology (Baltimore, Md. : 1950)

|July 12, 2015

Summary

Genetic deletion of microRNA-181a-1/b-1 (mir-181a-1/b-1) in T cells altered T cell receptor (TCR) signaling and selection. This manipulation increased T cell reactivity but did not induce autoimmunity, revealing microRNA control over immune tolerance.

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Development and Functional Characterization of Murine Tolerogenic Dendritic Cells

Development and Functional Characterization of Murine Tolerogenic Dendritic Cells

Published on: May 18, 2018

Area of Science:

Immunology
Molecular Biology
Genetics

Background:

T cell receptor (TCR) signaling is crucial for T cell development, function, and immune tolerance.
MicroRNAs (miRNAs) are key regulators of gene expression and have been implicated in immune cell biology.
The specific role of mir-181a-1/b-1 in modulating TCR signaling and its impact on T cell tolerance remains incompletely understood.

Purpose of the Study:

To investigate the consequences of genetically tuning TCR signaling on T cell selection, peripheral T cell function, and immune tolerance.
To elucidate the role of mir-181a-1/b-1 as a natural regulator of TCR signaling in vivo.
To determine how alterations in mir-181a-1/b-1 expression affect T cell reactivity and autoimmune disease induction.

Main Methods:

Genetic ablation of the mir-181a-1/b-1 gene in double-positive thymocytes.
Analysis of TCR and Erk signaling pathways.
Assessment of positive selection thresholds in the thymus.
Evaluation of naive T cell reactivity to self-antigens.
Induction and assessment of experimental autoimmune encephalomyelitis (EAE).
Measurement of basal TCR signaling and migration of peripheral T cells.

Main Results:

Genetic deletion of mir-181a-1/b-1 dampened TCR and Erk signaling and elevated the threshold for positive selection.
Loss of mir-181a-1/b-1 increased intrinsic reactivity of naive T cells to self-antigens but did not lead to spontaneous autoimmunity.
Absence of mir-181a-1/b-1 attenuated EAE induction, reduced basal TCR signaling in peripheral T cells, and decreased their migration to pathogenic sites.

Conclusions:

Immune tolerance can be modulated by microRNA gene products, specifically mir-181a-1/b-1.
Mir-181a-1/b-1 controls opposing activities in T cell selection and peripheral T cell function, thereby regulating immune tolerance.
Targeting microRNA pathways offers a potential strategy for modulating T cell responses in autoimmune diseases.