Impaired memory B cell IgG isotype switching and circulating T follicular-helper cell dysfunction in patients with chronic HIV-1 infection
Laila N. Abudulai
Abstract
Laila N. Abudulai
Abstract
HIV-induced dysfunction of B-cells and antibody production may contribute to impaired control of HIV replication. One mechanism by which HIV may evade protective antibody responses is to reduce opsonophagocytic antibody responses against HIV antigens by impairing memory B-cell isotype switching to lgG2 antibody production. This would also have the effect of increasing susceptibility to infection by pneumococci and other encapsulated bacteria. This thesis addresses the impact of B-cell and follicular-helper (TFH) cell depletion and dysfunction on switching of pneumococcal polysaccharide antibodies to lgG2 in HIV-1Infection.
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HIV-induced dysfunction of B-cells and antibody production may contribute to impaired control of HIV replication. One mechanism by which HIV may evade protective antibody responses is to reduce opsonophagocytic antibody responses against HIV antigens by impairing memory B-cell isotype switching to lgG2 antibody production. This would also have the effect of increasing susceptibility to infection by pneumococci and other encapsulated bacteria. This thesis addresses the impact of B-cell and follicular-helper (TFH) cell depletion and dysfunction on switching of pneumococcal polysaccharide antibodies to lgG2 in HIV-1Infection.
Key concepts: Isotype, Immunology, Immunoglobulin class switching, Memory B cell, B cell, Follicular phase, T cell, Antibody