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Humoral immune response primary

Ladies, G.S., et al., Evaluation of the primary humoral immune response following exposure of male rats to 176-estradiol or flutamide for 15 days, Toxicol. Sci., 46, 75, 1998. [Pg.59]

Pruett, S.B., Han, Y.-C., and Fuchs, B.A., Morphine suppresses primary humoral immune responses by a predominantly indirect mechanism, J. Pharmacol. Exp. Ther., 262, 923, 1992. [Pg.182]

As described previously, the humoral immune response results in the proliferation, activation, and subsequent production of antibodies by B cells following antigenic exposure and stimulation. The functionality and interplay between the three primary types of immune cells (macrophage, B cells, and T cells) required to elicit a humoral response can be assessed through various in vitro assays using cells from the peripheral blood or lymphoid tissues. [Pg.564]

Corticosteroids suppress both humoral and cellular immunity. Single doses produce a redistribution of lymphocytes with a concentration dependent decrease of CD4 and CDS positive cells. This in vivo lymphopenic effect correlates with the in vitro inhibition of stimulated T-cell proliferation. Furthermore, corticosteroids are able to inhibit the expression of genes coding for IL-1, IL-2, IL-6, interferon a, and tumor necrosis factor, TNE-a. Chronic administration decreases the size and also the cellu-larity of lymphoid tissues like lymph nodes, spleen, and thymus. Corticosteroids have more effect on the primary immune response and are less effective against previously sensitized immune responses. Their suppressive effects are more pronounced for T-cell immune responses than for the humoral immune response. [Pg.467]

Pasparakis M, Alexopoulou L, Episkopou V, Kollias G. Immune and inflammatory responses in TNFa-deficient mice A critical requirement for TNFa in the formation of primary B cell follicles, follicular dendritic cell networks and germinal centers, and in the maturation of the humoral immune response. J Exp Med 1996 184 1397-411. [Pg.376]

Goodman MG, Chemoweth DE, Weigle WO (1982) Potentiation of the primary humoral immune response in vitro by C5a anaphylatoxin. J Immunol 129 70-75. [Pg.688]

Recent evidence suggests that there are at least two subpopulations of Th cells, designated Thi and Th2- To date, the distinction between these two populations has been operationally defined and is based on the respective profiles of lymphokines which are produced whereas both Thi and Thi cells produce IL-3 and GM-CSF only Thi cells produce IL-2 and ILN-y, and only Thi cells produce IL-4, IL-5, IL-6, and IL-10. The importance of this phenomenon can be understood from the discussion of the primary effects of these lymphokines. By virtue of the production of IL-2 and ILN-y, Thi cells will facilitate the generation of a cell-mediated immune response. In contrast, Th2 cells will facilitate the generation of a humoral immune response by virtue of producing lymphokines which support B-cell function. Moreover, as indicated in Table 1, Thi cells can downregulate the activity of Th2 cells via the production of ILN-y, and Th2 cells can downregulate the activity of Thi cells via the production of IL-4 and IL-10. The basis for this cross talk between the two types of Th cells has been called the cytokine network. An important outcome of this cytokine network is that under certain conditions, a cell type traditionally characterized as a helper cell can actually suppress an immune... [Pg.1397]

Humoral immune responses can be divided into two types primary and secondary responses, which reflect the cellular dynamics of the immune system and the immune state of the host. A primary response is caused by the first exposure to a given immunogen and results in the appearance of predominantly IgM antibodies after a relatively long lag period, followed by a peak and a decline of antibody formation. After a lapse of time, another exposure to the immunogen produces a quite different, secondary response which is characterized by a shorter lag period, a stronger response with predominantly IgG antibodies and, after a peak has been reached, a slower decrease. [Pg.43]

CXCR5 Lack inguinal l5Tnph nodes, have small Peyer s patches, abnormal primary follicles, and lack germinal centers. B cells are diffusely distributed in T cell areas. Impaired humoral immune responses... [Pg.11]

Mild reductions in primary and secondary humoral immune response to immunization with exogenous protein antigen... [Pg.118]

LawrenceDA. 1981. Heavy metal modulation of lymphocyte activities. I./ vitro effects of heavy metals on primary humoral immune responses. Toxicol Appl Pharmacol 57 439-451. [Pg.467]

Primary response Humoral immune response that occurs when an antigen is first recognized by host B cells. [Pg.1170]

This chapter is concerned only with the primary defects in the cellular or humoral immune response. Thus, all hypercatabolic states or those due to exogenous agents, such as irradiation or drugs, are excluded as are im-munodeficient states secondary to malignant processes. The primary immunodeficiencies are categorized in the accompanying tabled... [Pg.230]

The primary function of the B lymphocytes is to produce antibodies, which are molecules that identify and lead to the destruction of foreign substances such as bacteria. The B lymphocytes and the antibodies they produce are responsible for humoral immunity. T lymphocytes provide immunity against viruses and cancer cells. These lymphocytes directly attack and destroy their targets by forming holes in the target cell membrane, causing cell lysis. The T lymphocytes are responsible for cell-mediated immunity. [Pg.232]

The marked decrease of the serum IgM in patients with Burkitt s lymphoma have been confirmed by Ziegler et al. (Zl) in East Africa, who noticed an impairment of the primary antibody response and low serum IgM levels in untreated patients with Burkitt s lymphoma, but not in patients in remission. They postulated a defect in humoral immunity possibly to impaired IgM synthesis. [Pg.214]

D. The boy has significantly reduced serum antibody levels and a reduced ability to mount an antibody response to childhood vaccinations. The most probably cause is a primary immunodeficiency disease affecting humoral immunity. [Pg.664]

Clearly, the immune response is an intricate sequence of events that involves a complex interaction between a number of cellular and humoral components. The overview provided here is just a brief summary of how some of the primary components participate in mediating acquired immunity. Readers are referred to additional sources for more information on this topic.16,18,49... [Pg.593]


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