Tingible body macrophage

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A tingible body macrophage. Tingible body macrophage.jpg
A tingible body macrophage.

A tingible body macrophage (TBMs) is a type of macrophage predominantly found in germinal centers, containing many phagocytized, apoptotic cells in various states of degradation, referred to as tingible bodies (tingible meaning stainable). [1] Tingible body macrophages contain condensed chromatin fragments. [2]

TBMs are licensed (empowered) for phagocytosis by follicular dendritic cells (FDCs). [3] FDCs provide TBMs with Milk fat globule-EGF factor 8 protein (Mfge8), which is a phosphatidylserine-binding "eat me" signal for removal of apoptotic germinal center B cells. [3]

It is thought that they may play a role in downregulating the germinal center reaction by the release of prostaglandins and hence a reduced B-cell induction of IL-2. [4]

Macrophages that contain debris from ingested lymphocytes are characteristic of a reactive follicular center in benign reactive lymphadenitis. Other accompanying signs of a benign follicular hyperplasia are well developed germinal centers with dark and light zones, in addition to numerous mitotic figures.

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Follicular B helper T cells

Follicular helper T cells (also known as follicular B helper T cells and abbreviated as TFH), are antigen-experienced CD4+ T cells found in the periphery within B cell follicles of secondary lymphoid organs such as lymph nodes, spleen and Peyer's patches, and are identified by their constitutive expression of the B cell follicle homing receptor CXCR5. Upon cellular interaction and cross-signaling with their cognate follicular (Fo B) B cells, TFH cells trigger the formation and maintenance of germinal centers through the expression of CD40 ligand (CD40L) and the secretion of IL-21 and IL-4. TFH cells also migrate from T cell zones into these seeded germinal centers, predominantly composed of rapidly dividing B cells mutating their Ig genes. Within germinal centers, TFH cells play a critical role in mediating the selection and survival of B cells that go on to differentiate either into long-lived plasma cells capable of producing high affinity antibodies against foreign antigen, or germinal center-dependent memory B cells capable of quick immune re-activation in the future if ever the same antigen is re-encountered. TFH cells are also thought to facilitate negative selection of potentially autoimmune-causing mutated B cells in the germinal center. However, the biomechanisms by which TFH cells mediate germinal center tolerance are yet to be fully understood.

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Follicular dendritic cell sarcoma (FDCS) is an extremely rare neoplasm. While the existence of FDC tumors was predicted by Lennert in 1978, the tumor wasn't fully recognized as its own cancer until 1986 after characterization by Monda et al. It accounts for only 0.4% of soft tissue sarcomas, but has significant recurrent and metastatic potential and is considered an intermediate grade malignancy. The major hurdle in treating FDCS has been misdiagnosis. It is a newly characterized cancer, and because of its similarities in presentation and markers to lymphoma, both Hodgkin and Non-Hodgkin subtypes, diagnosis of FDCS can be difficult. With recent advancements in cancer biology better diagnostic assays and chemotherapeutic agents have been made to more accurately diagnose and treat FDCS.

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Centroblast

A centroblast generally refers to an activated B cell that is enlarged and is rapidly proliferating in the germinal center of a lymphoid follicle. They are specifically located in the dark zone of the germinal center. Centroblasts form from naive B cells being exposed to follicular dendritic cell cytokines, such as IL-6, IL-15, 8D6, and BAFF. Stimulation from helper T cells is also required for centroblast development. Interaction between CD40 ligand on an activated T helper cell and the B cell CD40 receptor induces centroblasts to express activation-induced cytidine deaminase, leading to somatic hypermutation, allowing the B cell receptor to potentially gain stronger affinity for an antigen. In the absence of FDC and helper T cell stimulation, centroblasts are unable to differentiate and will undergo CD95-mediated apoptosis.

Follicular hyperplasia Medical condition

Follicular hyperplasia (FH) is a type of lymphoid hyperplasia and is classified as a lymphadenopathy, which means a disease of the lymph nodes. It is caused by a stimulation of the B cell compartment and by abnormal cell growth of secondary follicles. This typically occurs in the cortex without disrupting the lymph node capsule. The follicles are pathologically polymorphous, are often contrasting and varying in size and shape. Follicular hyperplasia is distinguished from follicular lymphoma in its polyclonality and lack of bcl-2 protein expression, whereas follicular lymphoma is monoclonal, and expresses bcl-2.

References

  1. Horst Ibelgaufts' COPE: Cytokines & Cells Online Pathfinder Encyclopaedia > tingible body macrophages Retrieved on June 27, 2010
  2. MacLennan I.C.M (1994). "Germinal Centers". Annual Review of Immunology. 12: 117–139. doi:10.1146/annurev.iy.12.040194.001001. PMID   8011279.
  3. 1 2 Aguzzi A, Kranich J, Krautler NJ (2014). "Follicular dendritic cells: origin, phenotype, and function in health and disease". Trends in Immunology . 35 (3): 105–113. doi:10.1016/j.it.2013.11.001. PMID   24315719.
  4. Smith JP, Burton GF, Tew JG, Szakal AK (1998). "Tingible body macrophages in regulation of germinal center reactions". Developmental Immunology. 6 (3–4): 285–294. doi: 10.1155/1998/38923 . PMC   2276033 . PMID   9814602.