Lymphocyte homing and immunology of extranodal lymphoid tissues
Franco Cavalli, Harald Stein, Emanuele Zucca in Extranodal Lymphomas, 2008
Lymphocytes continuously traffic from the blood through secondary lymphoid organs, where they search for their cognate antigen. The mechanism of entrance via blood is well understood also thanks to the generation of gene-targeted mice lacking central molecules required for entry.25,67–69 In contrast, the egress of lymphocytes from spleen or lymph nodes is recently starting to be elucidated. Retention and exit from lymphoid tissues is fundamental, because lymphocytes should be trapped in secondary lymphoid organs for receiving appropriate priming signals before leaving into medullary sinuses. Lymphocytes exit the spleen into the blood, and the LNs and PPs into the lymph. The mechanism of egression has been ascribed to the family of the sphingosine 1-phosphate (S1P) receptors. S1P, the ligand of S1P1 receptor, is found in high concentrations in blood and lymph, and is certainly implicated in the egression of lymphocytes, expressing the S1P1 receptor, from secondary lymphoid organs.70 Of note, FTY720, a small molecule agonist acting on several S1P receptor types, causes a reduction of lymphocytes in blood and tissues and their sequestration into lymphoid organs, which is independent of the chemokine receptors CCR7 and CXCR5.71–73 However, the detailed mechanisms of lymphocyte egression from lymphoid tissues remain to be clarified.
Benign Disorders of Leukocytes
Harold R. Schumacher, William A. Rock, Sanford A. Stass in Handbook of Hematologic Pathology, 2019
Based on clinical findings, the laboratory evaluation of lymphocytosis, particularly persistent lymphocytosis, may include any of the following studies: Blood smear examinationSerologic test(s) for infectious agent(s)Lymph node biopsy, particularly when serologic tests are nondiagnosticBone marrow examination, if a malignancy is suspectedCell marker studies, as needed, (a) to determine if the lymphocyte population is monoclonal (suggestive of malignancy) or polyclonal (nonmalignant) and (b) subclassify the lymphoid cells as T, B, common, and null. Assessment of maturational stage(s) of the cell-population of interest is also possible with specific cell marker studies. Such studies may be performed on blood, bone marrow, and/or lymph node specimensTest(s) for other suspected or identified underlying condition(s)
Bone Marrow
Wojciech Gorczyca in Atlas of Differential Diagnosis in Neoplastic Hematopathology, 2014
The lymphoid lineage also matures from the stem cell to the mature lymphocyte. A lymphocyte becomes either a B cell or a T cell. T cells are further subdivided into helper/inducer cells, suppressor/cytotoxic cells, and natural killer (NK) cells. The T cells regulate the B cells and kill the infected cells in the body. The B cells are programmed at birth to react against a specific glycoprotein sequence or antigen. Each B cell has a surface immunoglobulin (antibody) that contains a specific kappa or lambda light-chain configuration. If the B cell encounters its antigen match, it undergoes clonal expansion, making millions of its copies and eventually differentiating into a plasma cell. Plasma cells pour out their immunoglobulin antibodies from their cytoplasm into the serum, thereby enabling the infection or intruder proteins to be eliminated. Programmed cell death (apoptosis) as well as suppressor T cells prevents the clonal cells from becoming autonomous, and hence neoplastic.
Neutrophil-to-lymphocyte ratio in relation to the risk of all-cause mortality and cardiovascular events in patients with chronic kidney disease: a systematic review and meta-analysis
Published in Renal Failure, 2020
Wen-Man Zhao, Shu-Man Tao, Gui-Ling Liu
The lymphocyte is a kind of cell line with immune recognition function, mainly exists in the circulating lymph fluid in lymphatic vessels, and is an important cell component of the immune response function of the body. As the main enforcer of almost all the immune functions of the lymphatic system, lymphocytes are the frontline soldiers to fight against external infections and monitor the variation of cells in the body. Under stress, the release of cortisol and catecholamines in blood increases, which leads to bone marrow suppression, and thus the proliferation and differentiation of lymphocytes are reverentially regulated and the apoptosis of lymphocytes is aggravated. In a state of severe inflammation, hypo-lymphocytosis may even occur. Inflammatory response leads to lymphocyte apoptosis, lymphocyte differentiation, and down-regulated proliferation, and neurohumoral activation leads to a decreased immune regulation. In addition, lymphocyte counts have been used as indicators of nutritional status, and poor nutritional status is a risk factor for all-cause mortality [3,38].
Methotrexate-associated lymphoproliferative disorder with histopathological features of histiocytic necrotizing lymphadenitis
Published in Modern Rheumatology Case Reports, 2021
Shuko Kaito, Masashi Goto, Mikiko Iguchi, Yoshiaki Okuno, Koki Moriyoshi, Hiroshi Koyama
An 84-year-old Japanese woman who had been treated with MTX for RA for 15 years visited our hospital with complaints of general malaise and weakness of the extremities for 2 weeks. Cervical, axillary, and inguinal lymphadenopathy was found in the physical examination. Laboratory findings on her first visit showed significant thrombocytopenia, anaemia, elevated aminotransferases, and elevated CRP levels. Her peripheral blood contained some difficult-to-classify cells that we supposed were of lymphoid origin. The level of soluble interleukin-2 receptor (sIL-2R) was markedly elevated (12,061 U/mL). A computed tomography (CT) scan showed numerous enlarged systemic lymph nodes. We suspected MTX-LPD and withdrew MTX immediately. The patient was hospitalised and administered leucovorin (folic acid). Platelet transfusion was given on the first and third day in hospital. Bone-marrow aspiration showed normocellular marrow without lymphomatous lesions. Flow cytometric analysis revealed excessive proliferation of cells expressing T cell surface markers and no finding of B cell clonality. Cervical lymph node biopsy revealed a well-circumscribed area of necrosis showing abundant karyorrhectic nuclear debris. Around the necrosis, infiltration of histiocytes (CD68 positive in immunohistochemical staining) was seen. There were lymphoid cells in diverse maturation stages. These features were compatible with HNL (Figure 1). There was no formation of epithelioid cell granuloma, proliferation of atypical lymphocytes, or malignant cell growth. Immunohistochemical staining for CD3, CD5, CD10, and CD20 showed no evidence of malignant lymphoma.
Preliminary Report on Interleukin-22, GM-CSF, and IL-17F in the Pathogenesis of Acute Anterior Uveitis
Published in Ocular Immunology and Inflammation, 2021
Jerry Chien-Chieh Huang, Matthew Schleisman, Dongseok Choi, Claire Mitchell, Lindsey Watson, Mark Asquith, James T. Rosenbaum
The immune system is often conceptualized as having two arms, an innate component and an acquired or adaptive component. The latter contributors, primarily T and B lymphocytes, can undergo somatic gene rearrangements to make highly targeted immune responses. But the immune system also includes additional cells that have the light microscopic appearance of lymphocytes, but these lymphoid cells have limited or no ability to make gene rearrangements. These cells are often called innate lymphoid cells. Examples include natural killer cells (NKs), mucosal associated immune T cells (MAITs), and ILCs (innate lymphoid cells) which have been subdivided into ILC-1, 2, and 3 on the basis of the primary cytokines each produces. Natural killer cells express killer immunoglobulin-like receptor (KIR), polymorphic receptors which interact with major histocompatibility complex (MHC) class I. HLA B27 can dimerize on the cell surface and thus activate KIR.7 This has helped lead to a recognition that NK cells could contribute to HLA B27-related diseases such as ankylosing spondylitis.8 Much less is known about MAIT cells or ILC subsets in spondyloarthritis, except for a small number of studies now implicating ILC-3 cells.9,10 We are unaware of prior studies which have sought to investigate a role for MAIT cells or ILCs in the pathogenesis of acute anterior uveitis.
Related Knowledge Centers
- Adaptive Immune System
- Antibody
- B Cell
- Humoral Immunity
- Innate Lymphoid Cell
- Natural Killer Cell
- White Blood Cell
- Immune System
- T Cell
- Cell-Mediated Immunity