B-cell lymphoma pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Shivali Marketkar, M.B.B.S. [2]

Overview

Pathophysiology

Physiology

The normal physiology of B-cells can be understood as follows:

  • Development of mature B-cells include:
    • B-cells develop from hematopoietic stem cells originating from bone marrow. B-cell development occurs in the bone marrow through several steps including the ordered rearrangement of [[IGH@|Ig H] and L chain loci (i.e., VDJ recombination), positive selection, and negative selection.[1]
    • B-cell surface consists of membrane-bound Ig, complement component receptors, Fc receptors, and B cell-specific cell surface molecules representing by CDs (i.e., CD19, CD20, CD21, etc.).
    • Immature (transitional) B-cells migrate from the bone marrow to secondary lymphoid organs (i.e., lymph nodes, spleen) for activation. Activation begins with either T-cell dependent or T-cell independent. T-cell-dependent B-cell activation begins with the binding of the B-cell receptor (BCR) to the T-cell-dependent antigen. T-cell independent B-cell activation begins with BCR crosslinking through polysaccharides or via BCR and toll-like receptor (TLR) costimulation. Following the activation, further maturation steps including germinal center reaction (i.e., clonal expansion, class switch recombination, somatic hypermutation, affinity maturation) occur.[2][1]
    • B-cells can be divided into 3 main types include: B1 B-lymphoctes (originates from fetal liver), marginal zone (MZ) B2 B-lymphocyes, and follicular (FO) B2 B-lymphocytes.[3]
    • B-cells complete their maturation by differention into memory B cells or antibody-secreting plasma cells.
  • Functions of B-cells include:[1]

Pathogenesis

It is understood that there are different factors that have important roles in the pathogenesis of B-cell lymphomas including:[4]

Genetics

Chromosomal translocations involving the immunoglobulin heavy locus (IGH@) is a classic cytogenetic abnormality for many B-cell lymphomas, including follicular lymphoma, mantle cell lymphoma, diffuse large B cell lymphoma, MALT lymphoma, lymphoplasmacytoid lymphoma, multiple myeloma, and Burkitt's lymphoma. In these cases, The immunoglobulin heavy locus forms a fusion protein with another protein that has pro-proliferative or anti-apoptotic abilities. The enhancer element of the immunoglobulin heavy locus, which normally functions to make B cells produce massive production of antibodies, now induces massive transcription of the fusion protein, resulting in excessive pro-proliferative or anti-apoptotic effects on the B cells containing the fusion protein. Chromosomal translocations and mutations of tumor suppressor genes that are associated with B-cell lymphomas include:[4]

Associated Conditions

Conditions associated with B-cell lymphoma include:[4]

Gross Pathology

There is no gross pathologic finding characteristic of B-cell lymphoma.

Microscopic Pathology

Below is a microscopic image of a lymph node FNA specimen (Field's stain) of a patient with Hodgkin's lymphoma, a type of B cell lymphoma. The micrograph shows a mixture of cells commonly seen in Hodgkin's lymphoma:

  • Eosinophils
  • Reed Sternberg cells
  • Plasma cells
  • Histiocytes


Video

Shown below is a video of diffuse large B cell lymphoma {{#ev:youtube|9gEo7si6jtc}}

References

  1. 1.0 1.1 1.2 LeBien TW, Tedder TF (September 2008). "B lymphocytes: how they develop and function". Blood. 112 (5): 1570–80. doi:10.1182/blood-2008-02-078071. PMC 2518873. PMID 18725575.
  2. Hess C, Winkler A, Lorenz AK, Holecska V, Blanchard V, Eiglmeier S, Schoen AL, Bitterling J, Stoehr AD, Petzold D, Schommartz T, Mertes MM, Schoen CT, Tiburzy B, Herrmann A, Köhl J, Manz RA, Madaio MP, Berger M, Wardemann H, Ehlers M (September 2013). "T cell-independent B cell activation induces immunosuppressive sialylated IgG antibodies". J Clin Invest. 123 (9): 3788–96. doi:10.1172/JCI65938. PMC 3754242. PMID 23979161.
  3. Hoffman W, Lakkis FG, Chalasani G (January 2016). "B Cells, Antibodies, and More". Clin J Am Soc Nephrol. 11 (1): 137–54. doi:10.2215/CJN.09430915. PMC 4702236. PMID 26700440.
  4. 4.0 4.1 4.2 Küppers R (April 2005). "Mechanisms of B-cell lymphoma pathogenesis". Nat Rev Cancer. 5 (4): 251–62. doi:10.1038/nrc1589. PMID 15803153.


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