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Related Experiment Video

Updated: May 5, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

Mice lacking MHC class II molecules.

D Cosgrove¹, D Gray, A Dierich

¹Laboratoire de Génétique Moléculaire des Eucaryotes du CNRS, Unité 184 de Biologie Moléculaire de Génie Génétique de l'INSERM, Faculté de Médecine, Strasbourg, France.

|September 6, 1991

Summary

This summary is machine-generated.

Mice lacking major histocompatibility complex class II molecules show reduced CD4+ T cells and impaired B cell responses, confirming some roles but revealing novel aspects of lymphocyte differentiation.

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Area of Science:

Immunology
Molecular Biology
Genetics

Background:

Major histocompatibility complex (MHC) class II molecules are critical for T cell activation and immune responses.
Understanding the precise roles of MHC class II in T and B cell differentiation is essential for immunology.

Purpose of the Study:

To investigate the function of MHC class II molecules in T and B lymphocyte differentiation using genetically engineered mice.
To elucidate the impact of MHC class II deficiency on immune cell populations and functions.

Main Methods:

Generation of genetically modified mice lacking MHC class II antigens.
Flow cytometry analysis of T and B lymphocyte populations in spleen, lymph nodes, and thymus.
Assessment of B cell differentiation and antibody production.

Main Results:

Near-complete elimination of CD4+ T lymphocytes from peripheral lymphoid organs.
Presence of CD4 single-positive cells in the thymus, but not as mature thymocytes.
Normal B cell numbers and differentiation to plasma cells, but with aberrations like absent germinal centers and reduced IgG1 production.
Complete unresponsiveness to T-dependent antigens.

Conclusions:

MHC class II molecules are indispensable for the development and/or maintenance of CD4+ T cells in peripheral tissues.
While B cells can differentiate in MHC class II-deficient mice, their function is significantly impaired, particularly in T-dependent responses.
These findings confirm established roles of MHC class II but also highlight unexpected consequences of its absence in lymphocyte development and immunity.