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Immunological lessons from CD28 deficiency in humans.

Andreas Wieland¹, Rafi Ahmed¹

¹Emory Vaccine Center, Emory University School of Medicine, Atlanta, GA, USA; Department of Microbiology & Immunology, Emory University School of Medicine, Atlanta, GA, USA.

|July 9, 2021

Summary

This summary is machine-generated.

A mutation causing T-cell molecule CD28 deficiency leads to severe viral infections and poor vaccine response in three family members. This highlights CD28

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Area of Science:

Immunology and Molecular Biology
Human Genetics and Infectious Diseases

Background:

T-cell co-stimulation is crucial for adaptive immunity.
CD28 is a key T-cell co-stimulatory molecule essential for immune responses.
Genetic deficiencies in immune molecules can lead to severe clinical manifestations.

Purpose of the Study:

To investigate the clinical and immunological consequences of a mutation causing CD28 deficiency.
To analyze the susceptibility to specific viral infections in individuals with CD28 deficiency.
To evaluate the impact of CD28 deficiency on vaccine efficacy.

Main Methods:

Clinical case study of three affected family members.
Molecular genetic analysis to identify the mutation.
Immunological assays to assess T-cell function and viral loads.

Main Results:

Identified a mutation leading to a deficiency of the T-cell co-stimulatory molecule CD28.
Patients exhibited severe clinical symptoms, including infections with human papillomavirus-2 and -4.
Elevated levels of Epstein-Barr virus and cytomegalovirus were detected, alongside a poor response to vaccinations.

Conclusions:

CD28 deficiency severely impairs the immune system, leading to susceptibility to opportunistic viral infections.
The findings underscore the critical role of CD28 in maintaining immune homeostasis and effective vaccine responses.
This study provides critical insights into the pathogenesis of CD28-related immunodeficiency.