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Evaluation of T Follicular Helper Cells and Germinal Center Response During Influenza A Virus Infection in Mice
Published on: June 27, 2020
SAP is required for Th cell function and for immunity to influenza
Cris Kamperschroer1, John P Dibble, Dana L Meents
1Trudeau Institute, Saranac Lake, NY 12983, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|October 4, 2006
Summary
Signaling lymphocytic activation molecule-associated protein (SAP) is crucial for CD4 T cells to help B cell responses. SAP deficiency impairs plasma cell generation and antiviral immunity.
Area of Science:
- Immunology
- Molecular and Cellular Biology
Background:
- Antibody (Ab) responses are vital for immunity against infections.
- Defects in signaling lymphocytic activation molecule-associated protein (SAP) disrupt normal Ab production.
Purpose of the Study:
- To investigate the role of SAP in B cell and plasma cell responses.
- To elucidate the mechanism behind Ab defects in SAP-deficient individuals.
Main Methods:
- Analysis of B cell and plasma cell responses in SAP-deficient (SAP knockout (KO)) mice.
- Assessment of CD4 T cell function and T cell help for B cells.
- Evaluation of antiviral immunity following influenza virus challenge.
Main Results:
- SAP-deficient mice exhibit a CD4 T cell-intrinsic defect in generating Ag-specific plasma cells.
- SAP is essential for CD4 T cell-mediated B cell division, expansion, and T cell help.
- SAP deficiency leads to impaired humoral immune responses and susceptibility to influenza infection.
Conclusions:
- SAP in CD4 T cells is critical for T-dependent humoral immunity.
- SAP plays a key role in promoting antiviral immunity by supporting B cell responses.
- Restoring IgG through passive transfer protects against lethal influenza, highlighting SAP's importance.
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