Cellmediated immunity CMI

The current paradigm is that influenza A viruses are normally cleared from the infected lung by CD8 ", virus-immune cytotoxic T lymphocytes (CTLs). Lymphocytes of this subset are driven to recognize virally infected cells by antigen-presenting cells expressing viral peptides in the context of major histocompatibility complex (MHC) class 1 glycoproteins to the T cell receptor (TCR) and by subsequent interaction of the CDS molecule with the constant region of the MHC glycoprotein which is believed to increase the overall avidity of the interaction. Adoptive transfer experiments with T cell clones specific for one, but not another influenza A virus used to doubly infect mice, indicate that immune elimination depends on direct contact between the effector lymphocyte and the virus-infected target ceil. This is generally thought to operate via a Ca2 ' -dependent lytic degranulation pathway mediated by perforin and granzymes. There is no 'bystander' destruction of adjacent cells infected with the virus that is not recognized. Most cytolytic T cells are also capable of lysis by a largely Ca2+ and pore-forming independent mechanism utilizing as the Fas-Fas ligand interactions. Recent experiments have shown that CD8+ T cells can clear influenza virus via perforin/granzyme or Fas-dependent processes.

Immune CD4 1 T cells contribute to the lung consolidation characteristic of influenza pneumonia, and also play a significant role in virus clearance. Cloned,

CD4 T cell lines can eliminate virus from the lung in the apparent absence of primed CDS lymphocytes. Cytolytic CD4 T cells can be generated in vivo, though such generation is dependent on depletion of CD8 T cells. The Fas-Fas ligand pathway of cytolysis is believed to have a more prominent role in CD4 1 versus CD8 T cell-mediated cytotoxicity.

The one task that can be definitely atributed to the CD4 1 population is help for antibody production, which is now known to be the mechanism underlying the clearance is now known to lung by the CD4" clones. A major role of CD4- T cells specific for viral peptides associated with MHC class II glycoproteins on B cells is primarily the generation of 'helper' cytokines such as interleukin 4 (II.-4) and H.-5. These cytokines promote the clonal expansion and differentiation of B cells to antibody-secreting plasma cells.

The inflammatory exudate that can be lavaged from the respiratory tract of mice with influenza is dominated by macrophages, natural killer (NIK) cells and T lymphocytes, with the CD8 + subset being 2-3 times more prevalent than the CD44 cells. Macrophage recruitment and activation occurs in the absence of the CD4' population and is dependent on nonspecific chemokine/cytokine recruitment probably produced from infected respiratory epi-thelia. The number of T cells in the exudate declines rapidly from the time that it is no longer possible to recover infectious virus. A role for NK cells in mediation of virus clearance has not been well established. Major questions concerning the nature of influenza pneumonia include the relative roles of different lymphokines, cytokines and chemokines in the disease process.

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