Infection with any influenza A virus primes for a secondary CD8+ T cell response to any other influenza A virus. This reflects that many of the CD8+ T cells are specific for peptides of conserved, internal virus proteins presented on the cell surface in the binding site of self MHC class I molecules. The NP is particularly prominent in this regard, though the M protein, nonstructural protein (NS1), and even the viral polymerases (PA, PB1-2) may contribute to antigenicity. The significance of a particular viral peptide depends on whether or not it binds to the MHC class I glycoproteins expressed in the individual at risk. Presence of these cross-reactive memory T cells has been correlated with less severe disease and their absence is probably the reason why influenza tends to be more lethal in very young children and in the elderly. Mouse experiments using limiting dilution analysis (LDA) suggest that following infection, increased numbers of CD44 or CD8' T cells persist in lymphoid tissue for life. CD8 1 T cell clonotypes that survive in the long term have virus-specific frequencies at least 30-times those found in naive animals, and express characteristic profiles of adhesion and activation antigens such as CD44 and CD62L. These cell surface molecules are believed to influence lymphocyte recirculation and homing.
Influenza-immune CD4+ helper T cells are specific for viral peptides presented in the context of self MHC class II glycoproteins. Following infection, the normal sequence of events is that antigenic determinants on the viral coat glycoproteins are bound by lg receptors on appropriate B lymphocytes. This leads to the interiorization of the virus-Ig complex, degradation in lysosomes, and expression of constituent peptides + MHC class II molecules on the surface of the B cell. Lymphokines, such as IL-2 and IL-4, that are needed to promote the growth and differentiation of B lymphocytes specific for the influenza hemagglutinin (HA) molecule, can thus be provided by T helper cells reactive to epitopes derived from any of the viral proteins. This may be one reason why whole, inactivated influenza virus vaccines are more effective than, for instance, those consisting solely of HA subunits.
See also: Antigen-binding site; Antigen presentation via MHC class I molecules; Antigen presentation via MHC class II molecules; Antigenic variation; B lymphocytes; MHC, functions of; T lymphocytes; Vaccines; Vaccines, adverse reactions to; Viruses, immunity to.
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