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. 2013 Feb;9(1):13–22. doi: 10.2174/1573395511309010003

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© 2013 Bentham Science Publishers

This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. (2) — Hypothetical model of lymphoma development in SS patients. The transition from autoimmune state to lymphoma is a multi-step process and that chronic stimulation by exoantigen or autoantigen plays an important role in the development of lymphoma by driving the proliferation of specific B cells and increasing the frequency of their transformation. Inflammation: Infiltration of CD4+ T cells, memory B cells and dendritic cells in the minor salivary glands perpetuate chronic inflammation. (Polyclonal B cell proliferation: Increased production of BAFF and IFNs in SS patients cause polyclonal B cell proliferation and thereby contribute to the characteristic pattern of myoepithelial sialadenitis (MESA) or benign lymphoepithelial lesion. Oligoclonal B cell proliferation: BAFF specifically regulates B lymphocyte proliferation and survival, altered B cell differentiation. Chronic stimulation by exoantigen or autoantigen may drive the proliferation of specific B cells through restricted usage of immunoglobulin heavy chain complementarity determining region 3 (IgVH-CDR3) and increasing the frequency of their transformation. Monoclonal B cell proliferation: During B cell development, immunoglobulins undergo recombination, somatic mutation and isotype switching. These events may increase the risk of translocation of oncogenes such as Bcl-2 and c-Myc to immunoglobulin loci (chromosome 14q32). Transformation to high grade malignancy: Defect of P53 tumor-suppressor activity, high frequency of t(14,18) translocation, amplification of bcl-2 and/or c-Myc, and trisomy 3 may facilitate the progression of low-grade MALT lymphoma to more malignant high-grade lymphoma.