Multiple myeloma is a heterogeneous group of malignant clonal
B-lymphocyte neoplasms of terminally differentiated bone marrow plasma cells.
The mechanisms include depression of genetic material, transformation of progenitor cell before its full diversity of
B-lymphocyte pathway, and a neoplastic expansion of normal B cells that describe T-cell antigens.
CD22 is a
B-lymphocyte restricted transmembrane protein with a higher receptor density in HCL cells relative to normal B cells, making it an attractive therapeutic target for the treatment of this cancer.
These include 1) the
B-lymphocyte, which stimulates B-cells to produce antibodies and helps alert T-lymphocytes; and 2) the T-lymphocyte, which stimulates T-cells to destroy compromised cells in the body and helps alert other leukocytes to start attacking.
In addition,
B-lymphocyte stimulator has the potential to exacerbate the disease by activating other cells through tumor necrosis factor and numerous other mediator secretions.
These neoplasm arise when a cell of
B-lymphocyte plasma cell lineage proliferates to form a malignant population of similar cells.
Filleron et al., "Human solid tumors contain high endothelial venules: association with T- and
B-lymphocyte infiltration and favorable prognosis in breast cancer," Cancer Research, vol.
This is an extremely uncommon finding, as the tropism of EBV for
B-lymphocyte has been associated with B-cells cancers, including Burkitt, Hodgkin, and diffuse large cell lymphomas [14,15]; conversely EBV-positive T-cell lymphoma is exceedingly uncommon in western populations and has been attributed either to a possible antiapoptotic action exerted by the viral DNA hosted in the infected T-cells and/or to signals transmitted by some viral proteins such as Latent Membrane Protein 1 causing the continuous stimulation of members of the TNF receptors [2,16].
When SAP is bound to the cytosolic SLAM, it is thought to enhance T- and
B-lymphocyte proliferation, CD8+ T cell activation by antigen-presenting B cells, T-lymphocyte cytokine secretion, and
B-lymphocyte antibody production [2, 3].
These facts also support the hypothesis that CVID-associated
B-lymphocyte defects and hypogammaglobulinemia give rise to decrease of sex hormone-binding globulin and sex hormone receptor; consequently, sex hormone cannot effectively promote the periodical change of endometrium [Figure 1].{Figure 1}