T and B lymphocytes

The adaptive or specific arm of the immune system consists of T- and B-lymphocytes and antibodies. T- and... 

Cellular Components of Adaptive Immune Responses are T- and B-Lymphocytes whereas Humoral Components are Antibodies. 

The hallmark of T- and B-lymphocytes is that each single lymphocyte expresses antigen receptors of a single specificity that was created randomly during the development of that individual lymphocyte. This is achieved mainly by sequential genetic rearrangement... 

Lymphocytes are specialized white blood cells that play a crucial role in an immune response.They can be T lymphocytes, which can directly target and destroy defective cells, or B lymphocytes, which produce antibodies directed against specific antigens. Both T and B lymphocytes produce a variety of cytokines to augment and amplify the immune response. 

Multiple scelerosis is an autoimmune disease mediated by T and B lymphocytes and macrophages. This is characterized by extensive inflammation and demyelination of the myelin sheath that surrounds the nerve fiber. The death of the nerve fiber results in a variety of symptoms that can lead to impairment of movement, paralysis, and death. 

Cerqueira, F. Corderio-Da-Silva, A. Gaspar-Marques, C. Simoes, F. Pinto, M. M. M. Nascimento, M. S. J. Effect of abietane diterpenes from Plectranthus grandidentatus on T- and B-lymphocyte proliferation. Bioorg. Med. Chem. 2004, 12, 217-223. 

Nombela-Arrieta C, Lacalle RA, Montoya MC, et al. Differential requirements for DOCK2 and phosphoinositide-3-kinase gamma during T and B lymphocyte homing. Immunity 2004 21(3) 429 141. 

Lymphocytes are of two sizes smaller lymphocytes, with a diameter of 6-8 pm, and larger lymphocytes, with a diameter up to 18 pm. They are found not only in blood, but in lymph and in every tissue of the body. Larger lymphocytes are believed to be cells that differentiate into T and B lymphocytes when activated by specific antigens. The life span of lymphocytes may vary from a few days to many years. Lymphocytes have been suggested as potential carriers for transporting macromolecules, particularly DNA, to other cells. Low molecular weight exogenous substances can be introduced into lymphocytes by electrical breakdown methods. 

In addition to the classical stress hormones already reviewed, several other hormones are augmented in response to stress. Stress-induced prolactin release is one of the most frequently studied examples. There is no doubt about the causal relationship between stress and increased pituitary prolactin release, but the biological meaning is much less clear (G2). This phylogenetically old hormone has been shown to have more than 85 different functions in all vertebrate species. However, besides its role in the induction of maternal lactogenesis, the physiological importance of prolactin is at present not fully established. Experimental and clinical evidence supports the view that prolactin is also an immunoregulating hormone (M44, R18). Prolactin receptors are present on human T and B lymphocytes (R18), and T lymphocytes depend on prolactin for maintenance of immunocompetence (B19). In addition, it has been shown that prolactin is able to influence the devel-... 

Most cytokines are pleiotropic, i.e. can affect a variety of cell types. Moreover, the effect that a cytokine has on one cell type may be the same or different to its effect on a different cell type. IL-1, for example, can induce fever, hypotension and an acute phase response. G-CSF is a growth factor for neutrophils, but it is also involved in stimulating migration of endothelial cells and growth of haematopoietic cells. IFN-y stimulates activation and growth of T- and B-lymphocytes, macrophages, NK cells, fibroblasts and endothelial cells. It also displays weak anti-proliferative activity with some cell types. 

IFN-y also directly modulates the immune response by affecting growth, differentiation and function of both T- and B-lymphocytes. These effects are quite complex and are often influenced by additional cytokines. IFN-y acts as a growth factor in an autocrine manner for some T cell sub-populations, and it is capable of suppressing growth of other T cell types. It appears to have an inhibitory effect on development of immature B-lymphocyte populations, but it may support mature B cell survival. It can both up-regulate and down-regulate antibody production under various circumstances. 

Additional molecular mechanisms must also mediate IFN-y effects, as it promotes a marked clinical improvement in some CGD patients without enhancing phagocyte activity. IFN-y s demonstrated ability to stimulate aspects of cellular and humoral immunity (e.g. via T- and B-lymphocytes), as well as NK cell activity, is most likely responsible for these observed improvements. 

Another early genetic disease for correction by gene therapy was SCID. One form of this disease is caused by a lack of adenosine deaminase (ADA) activity. ADA is an enzyme that plays a central role in the degradation of purine nucleosides (it catalyses the removal of ammonia from adenosine, forming inosine, which, in turn, is usually eventually converted to uric acid). This leads to T- and B-lymphocyte dysfunction. Lack of an effective immune system means that SCID sufferers must be kept in an essentially sterile environment. 

In summary, although numerous AhR-dependent changes in the bone marrow and thymus have been found in TCDD-treated mice, it appears that these effects are self-limiting in adult mice, as T and B cell numbers are not reduced in secondary lymphoid tissue except after exposure to high doses of TCDD or in the context of an adaptive immune response. More subtle effects, such as changes in the antigenic specificity of peripheral T and B lymphocyte populations, have not been documented. 

This drug has marked immunomodulatory effects and can alter the normal function of T and B lymphocytes, NK cells and macrophages, both in vivo and in vitro, in humans and animals (Table 30.1).910 Although the molecular and cellular mechanisms for these effects are not fully defined, it is believed that both receptor and non-receptor mechanisms are involved. Cannabinoid receptors (CBRs) are G-protein coupled 7-... 

Acid acetone extracts of human and rodent leukocytes (RBL-cells) have been found to contain immunoreactive SOM (iSOM) and immunoreactive SP (iSP) as determined by radioimmunoassay [144], Quantities of the peptides varied from 325 pg iSOM/107 cells for human monocytes and 272 pg iSOM/107 cells for RBL-cells to 4.4 pg iSOM/107 cells for human T cells. iSP was highest in murine bone marrow-derived mast cells (64 pg iSP/107 cells) and RBL-cells (23 pg iSP/107 cells) and lowest in human T and B lymphocytes (2.5 and 1.2 pg iSP/107 cells, respectively). Interestingly, the murine bone marrow-derived mast cells had the highest ratio of iSP to iSOM. Preliminary chromatographic results show a large and a small SOM (SOM-28 and SOM-14, respectively). SOM-14 (3 x 10 9 M) has been shown to inhibit histamine release and LTC4 generation from murine bone marrow-derived mast cells stimulated by anti-IgE serum [144]. 

Infection is the most common cause of morbidity and mortality in MDS patients, accounting for 40-60% of deaths in various studies. The common infections are those normally associated with neutropenias, such as Gramnegative septicaemia and bacterial bronchopneumonias. Indeed, most MDS patients are neutropenic at some stage in their disease. Even those who do not have a neutropenia may have a defect in their neutrophil function. Many patients have clearly-defined defects in T- and B-lymphocyte functions, and variable defects in monocyte numbers or function have been described. Disorders of neutrophil function are common. Many reports indicate that phagocytosis, chemotaxis, respiratory-burst activity and degranulation are defective in some MDS patients, and hypogranulation is often observed. 

Finally, ASM may be central to the response to y-irradiation in vitro and in vivo, in some cells. A requirement for ASM for release of ceramide upon irradiation has been observed in T- and B-lymphocytes (Santana et al. 

The classical cellular sources of histamine are mast cells and basophils, gastric enterochromaffin-like cells, platelets and histaminergic neurons. Interestingly the cells in the immune system, which do not store histamine, show high HDC activity and are capable of production of high amounts of histamine, which is secreted immediately after synthesis [20]. These cells include platelets, monocytes/macrophages, DCs, neutrophils, and T and B lymphocytes. 

It now appears certain that destruction of malaria parasites in vivo depends in part, if not wholly, upon the presence of humoral antibodies, and this must explain the success achieved with the passive transfer experiments. The exact role of the T and B lymphocytes in immunity in malaria infection in man still needs clarification. In rats the ability to resist P. berghei infection seems to be thymus dependent, and higher parasitemias were encountered in the thymectomized rats, which also developed severe anemia (B6). 

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