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The CD40 antigen and its ligand

J Banchereau¹, F Bazan, D Blanchard

¹Schering-Plough, Laboratory for Immunological Research, Dardilly, France.

Annual Review of Immunology

|January 1, 1994

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CD40, a protein on B cells and other cells, interacts with CD40-L on T cells to drive B cell proliferation and antibody production. This interaction is crucial for generating memory B cells and is implicated in immune disorders like hyper-IgM syndrome.

Area of Science:

Immunology
Cell Biology
Molecular Biology

Background:

CD40 is a transmembrane protein belonging to the tumor necrosis factor receptor superfamily.
It is expressed on various immune cells, including B lymphocytes and dendritic cells, as well as non-immune cells like epithelial cells.
CD40 interacts with its ligand, CD40-L, a molecule found on activated T cells and other cell types.

Purpose of the Study:

To elucidate the role of CD40 and its ligand (CD40-L) in immune cell activation and function.
To investigate the downstream effects of CD40-CD40-L interactions on B cell proliferation, differentiation, and antibody isotype switching.
To explore the implications of CD40 signaling in the generation of B cell memory and its relevance to diseases such as X-linked hyper-IgM syndrome.

Main Methods:

Related Experiment Videos

Analysis of CD40 and CD40-L gene mapping and protein characteristics.
In vitro studies involving cross-linking of CD40 with anti-CD40 or CD40-L expressing cells.
Investigation of B cell responses, including proliferation, immunoglobulin secretion, and isotype switching, in the presence of cytokines like IL-4, IL-10, and TGF-beta.
Examination of the consequences of CD40-L deficiency in X-linked hyper-IgM syndrome.

Main Results:

Cross-linking CD40 on B cells induces significant proliferation and, with IL-4/IL-13, leads to long-term B cell lines and IgE secretion.
IL-10 promotes high immunoglobulin production with limited proliferation, inducing naive B cells to produce IgG3, IgG1, and IgA1, further enhanced by TGF-beta for IgA2.
CD40-dependent activation is critical for memory B cell generation, evidenced by phenotype acquisition, isotype switching capabilities, and the absence of germinal centers and specific immunoglobulin classes in CD40-L deficient individuals.

Conclusions:

CD40-CD40-L interaction is a key pathway for B cell activation, proliferation, differentiation, and memory formation.
This signaling axis plays a vital role in normal humoral immunity, including immunoglobulin class switching and the generation of long-lived plasma cells and memory B cells.
Dysregulation of the CD40-CD40-L pathway leads to severe immunodeficiencies, highlighting its critical importance in adaptive immunity.