Pathophysiology of polyclonal gammopathy
Polyclonal hypergammaglobulinemia is usually due to an underlying infectious, inflammatory or neoplastic disorder such as a carcinoma. Antigen is processed by antigen-presenting cells which activate T cells to induce proliferation of antigen-specific B cells. Under the influence of cytokines such as interleukin 6 (IL-6), these B cells differentiate into antibody-producing plasma cells. These polyclonal plasma cells increase in number in the bone marrow, gut, lymph nodes, spleen and liver. They produce electrophoretically heterogeneous immunoglobulins which are detected in the serum as a broad increase, chiefly in the gamma globulin band. The polyclonal increase in immunoglobulin reflects expansion and differentiation of plasma cells, collectively producing more than one isotype of immunoglobulin (Ig) heavy chain. Both k and \ light chains arc represented. Rarely, no underlying cause is found, and the increase is attributed to an unknown antigen exposure or defective regulation of B cell proliferation and differentiation. The increase in plasma cells and gamma globulin almost never causes symptoms. The presence of symptoms reflects the specific underlying disease.
Rarely, the polyclonal hypergammaglobulinemia may be restricted to one or more subclasses of immunoglobulin (Ig). Hyper-IgM syndrome is described in another article in the encyclopedia. Hyper-IgE, or Job's syndrome, is characterized by a polyclonal increase in IgE alone. In these patients the catabolic destruction of IgE is slowed. The primary
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