The effector function of platelets is induced and regulated by T lymphocytes (original) (raw)
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Activation of lymphocytes after platelet allotransfusion possessing only class I MHC product
Clinical and Experimental Immunology, 2008
SUMMARYAfter platelet allotransfusion, we found a characteristic increase in the expression of interleukin-2 receptor, dipeptydilpeptidase IV (CD26), activation-inducer molecule (AIM, CD69) and transferrin receptors (CD71) on day 3 indicating that important functional molecules expressed on the activation of lymphocytes by allogeneic platelets. At the same time, no consistent increase of other activation molecules such as Ki-1 (CD30), intercellular adhesion molecule (ICAM-1, CD54) and Ki-24 (CDw70) antigen expression was detected, probably as a result of the selective activation of some lymphocyte subsets. In order to obtain further evidence for the in vivo activation triggered by allogeneic platelets, a subsequent step of T cell activation towards differentiation was investigated with monoclonal antibodies to leucocyte common antigens. A sharp expression of the UCHL1, coupled with a decrease of the CD45R molecule was detected on day 7 or 14, suggesting a T cell priming.
Characterization of the T-lymphocyte response elicited by mouse immunization with rat platelets
Experimental Hematology, 2011
Objective. Immunization of normal CBA mice with rat platelets leads to an autoantibody response directed against mouse platelets. The purpose of this work was to determine the involvement of T lymphocytes in this response. Materials and Methods. T-lymphocyte responses were analyzed in vivo by depletion and transfer experiments and ex vivo by proliferation assay and cytokine measurements. Results. Mouse immunization with rat platelets induced production of antibodies reacting with rat and mouse platelets. This response was found to depend on CD4 + T-helper lymphocytes reacting with rat, but not with mouse platelets. These anti-rat platelet T-helper cells were mainly of the Th1 phenotype. When transferred into na€ ıve mice, they enhanced the anti-mouse platelet antibody response induced by subsequent immunization with rat platelets. In addition, depletion of CD25 + cells enhanced the thrombocytopenia induced by immunization with rat platelets, whereas adoptive transfer of CD4 + CD25 + cells from immunized mice suppressed it. Conclusions. Our results suggest that activation of anti-rat platelet T-helper cells can bypass the mechanism of tolerance and result in the secretion of autoreactive antibodies, but this response is still controlled by regulatory T cells that develop progressively after immunization. Ó Ca mice were purchased from Harlan (Horst, The Netherlands). They were used when they were 8 to 12 weeks old. Wistar rats were bred in our local facility by J-P. Dehoux. The project was approved by the local commission for animal care.
Journal of Experimental Medicine, 1972
We have studied the leukocyte-dependent mechanism of histamine release (LDHR) from rabbit platelets, a complement-independent mechanism which has been implicated in the deposition of immune complexes in acute serum sickness of rabbits. It was found by chromatography and passive transfer of serum from immunized rabbits that the antibody responsible for the LDHR was of IgE type. By electron microscope study of the reaction, the leukocyte involved in agglutination of platelets and release of their histamine content was identified as the basophil. Upon addition of antigen, basophils sensitized with IgE degranulated, released their histamine content and a platelet-activating factor (PAF) that caused aggregation of platelets and release of their histamine. Conditions of preparing and preserving PAF activity and some properties of this factor have been elucidated. LDHR must, therefore, be considered as an immediate hypersensitivity-type mechanism which may link allergic reactions with immu...
Chapter 5 Platelet Interactions with Viruses and Parasites
2017
Over the last few years our understanding of the role of platelets has evolved. While originally considered to be solely involved in thrombus formation recent studies suggest that they play an important role in the innate immune system. As the most numerous particles in the blood platelets are the first responders to any breaches in the vasculature where they bind to the damaged vessel and aggregate to seal the leak. They also become activated and secrete the contents of their granules, which contain anti-microbial peptides, which acts to sterilise the wound and to recruit other immune cells. As a result thrombocytopenia is a common response to infection by many different organisms [1, 2].
(5) The role of lymphokines or gamma (γ) interferon in host defense of chickens to Eimeria tenella
Veterinary Parasitology, 1988
We have determined that cercariae/young schlstosomules and adults of Schistosoma mansom synthesize a wide range of elcosanolds when stimulated with hnoleic acid-an essential fatty acid. Cercariae (young schistosomules of 1 h old) secrete 64%, while adults secrete over 80% of synthesized eicosanoids. On a mg-~ soluble protein basis, eicosanoid secretion is ordered as follows: adult females > adult males > > > cercariae. One mature adult worm pair secrete approximately 4.36 ng PGE, 3.41 ng LTB4 and 15.13 ng 5-HETE as determined by RIA. Results of HPLC have determined that 15-HETE is the major HETE species secreted by adults and cercanae. The direct immunoregulatory capacities of various emosanolds are now just beginning to be understood and it is increasingly clear that they are potent immunoregulators in addition to their classically defined functions as vasoconstrmtors, vasodilators, platelet aggregators and inflammatory agents. The HETEs and HPETEs of the 5, 11 and 12 series are known to promote lymphocyte proliferation, while 15-HETE inhibits mitogen-induced lymphocyte proliferation and inhibits IL-2 production. In addition, it has been reported that LTB4 mduces the activation of human suppressor cells, and various leukotnenes are known to be both mhibitors and promoters of leukocyte and lymphocyte chemotaxls or chemokmesls. The cyclo-oxygenase products, PGE2 and PGE1, are also known to have immunoregulatory properties. Ceuppens and Goodwm (1984), m their review on PG modulatmn of lymphocytes, state that physiologmal concentrations of PGE suppress most characteristics of T-lymphocyte activation in vitro, as well as inhibit B-cell proliferatmn. Thus, the literature supports the concept that eicosanoids can modulate the immune system both as local inflammatory or anti-inflammatory agents and leukocyte chemotachc lnhibitors and promoters, as well as have direct effects on T-and B-cell activatmn and prolfferatmn. Currently, the hterature on host immune evasion by schistosomules and adults of S mansoni has emphasized antigen acquisition and antigen shedding as plausible mechamsms, as well as an unidenhfied mtrmsm defense mechamsm in schistosomules. We postulate that part of the defense mechanism m cercarme/schistosomules and adults may involve secretion of immunosuppressant eicosanoid species. (Supported by U.S. Army Med. Res. Dev. Cmd. No. DAMD17-85-C-5180.)
The Journal of …, 1986
Evidence is accumulating that antibody dependent, cell-mediated cytotoxicity (ADCC) plays a critical role in the mechanisms of defense against schistosomes (1, 2). In several experimental models and in the human situation, the participation of phagocytic cell populations, including macrophages, eosinophils, and platelets, has been demonstrated (3-6). Killing in vitro of schistosomula, the main targets of immune attack, is observed when these cells interact with the parasite in the presence of specific antibodies (3, 5-9). During experimental rat schistosomiasis, or during human infection, large variations in the cytotoxic activity of eosinophils attributable to immune complexes may occur (7, 10), and it has been shown (10) that immune complexes isolated from rat infection serum can either activate or inhibit schistosomulum killing by normal eosinophils. More recently, the production of Schistosoma mansoni-specific mAbs has allowed an alternative explanation for variations in the capacity of different sera to support killing (11). A rat IgG2c mAb (IPLSm3), which did not exhibit any killing activity for schistosomula, specifically inhibited the eosinophil-dependent cytotoxicity mediated by an IgG2a mAb (IPLSm 1) (11). The blocking effect of IgG2c was dual, both at the surface target antigen (M r 38,000) and at the effector cell level, by competition for the Fry receptor (12, 13). IgG2c antibodies were also able to inhibit the in vivo protection conferred by IgG2a mAbs. The demonstration of such mechanisms in the rat raises the question of the possible existence in human schistosomiasis of blocking antibodies modulating the efficiency of immune effector mechanisms (14). To test such a hypothesis, we have studied a group of infected children who are involved in epidemiologic and immunologic studies of schistosome infection (15, 16). Among this group, two subgroups have been distinguished. The first, one of 22 children showing