Production of growth factors (PDGF & TGF-beta) at the site of tissue repair.
Explore the source record for details and available documents.
Animals↗
Biomedical subjects
C A Grotendorst
Publications and source records attributed to C A Grotendorst.
Complement effects of the infectivity of Plasmodium gallinaceum to Aedes aegypti mosquitoes. II. Changes in sensitivity to complement-like factors during zygote development.
During transformation into ookinetes, the zygotes of Plasmodium gallinaceum are initially resistant to lysis by heat-labile and EDTA-sensitive factors in the serum of their natural host, the chicken. Between 6 and 8 hr postgametogenesis, zygotes cultured in vitro lose their resistance to these factors. Loss of resistance to these factors in vitro is reflected by loss of infectivity of the zygotes to Aedes aegypti mosquitoes in the presence of native chicken serum. These factors are probably components of the alternative pathway of complement (APC) of chicken serum. Gametocytes of P. gallinaceum in chicken blood are able to infect A. aegypti mosquitoes apparently due to inactivation of the APC in a blood meal within 3-4 hr after ingestion, i.e., several hours before the zygotes lose their resistance to chicken APC. In addition to the heat-labile factors (APC) in chicken serum, the zygotes are transiently sensitive to other factor(s) in the mosquito blood meal. These factor(s) are not destroyed by prior heating of the chicken serum given in a blood meal and therefore cannot be complement components. The antiparasitic effects of the factors are neutralized by addition of EDTA to the blood meal and could be due to an EDTA-sensitive metalloprotease present in the mosquito midgut.
Aedes↗
Fibroblast heterogeneity in scleroderma: Clq studies.
Fibroblast heterogeneity has been the basis of a pathogenetic theory of scleroderma in which one subpopulation of high collagen producing cells is expanded by selective growth. In studies by others using gingival cells, fibroblast membrane Clq receptor affinity correlates positively with collagen production. We have demonstrated distinctly higher amounts of Clq binding of fibroblasts from 2 patients with early scleroderma compared to late scleroderma and controls. These observations are consistent with the overgrowth of a normally occurring subpopulation of cells and provide support for clonal selection in the pathogenesis of scleroderma.
Adult↗
Complement effects on the infectivity of Plasmodium gallinaceum to Aedes aegypti mosquitoes. I. Resistance of zygotes to the alternative pathway of complement.
Gametocytes are the intraerythrocytic stages of malaria parasites that infect mosquitoes. When gametocytes of the chicken malaria parasite Plasmodium gallinaceum are ingested by a mosquito they become extracellular in the mosquito midgut, form gametes, and fertilize within 10 to 15 min after the insect has taken a blood meal. Gametocytes of P. gallinaceum were infectious when fed to Aedes aegypti mosquitoes in blood meals containing native serum from chickens or from the non-host species, man or sheep. Gametocytes stimulated to undergo gametogenesis and to fertilize in vitro were also infectious when fed to mosquitoes in native chicken serum. However, native serum from most non-host species, including sheep and man, suppressed the infectivity of newly fertilized zygotes to mosquitoes and lysed the zygotes in vitro. These effects were shown to be due to the activity of the alternative pathway of complement (APC) in the serum of the non-host species. After mild trypsin treatment, the zygotes of P. gallinaceum no longer infected mosquitoes in the presence of native chicken serum, although in heat-inactivated chicken serum their infectivity was normal. We conclude that trypsin-sensitive components on the zygotes surface protect them from destruction by the APC of their native host. The ability of gametocytes of P. gallinaceum to infect mosquitoes in the presence of native human serum is probably due to proteases that inactivate the APC of human serum before the gametes and zygotes emerge as extracellular parasites in the blood meal.
Aedes↗
Target antigens in malaria transmission blocking immunity.
Malaria transmission blocking immunity has been found to operate against two distinct phases of development of malaria parasites in the mosquito midgut: (i) against the extracellular gametes and newly fertilized zygotes shortly after ingestion by a mosquito of parasitized blood and (ii) against the zygotes during their subsequent development into ookinetes. Immunity is antibody-mediated and stage-specific. A set of three proteins, synthesized in the gametocytes, expressed on the surface of the gametes and newly fertilized zygotes and subsequently shed during later transformation of the zygotes, has been identified as the target antigens of anti-gamete fertilization blocking antibodies. A single protein, synthesized and expressed on the zygote surface during its development to ookinetes, has been identified as the target of antibodies which block the development of the fertilized parasites in the mosquito. Immunization of human populations against gamete or zygote antigens, while not directly protecting an immunized individual from inflection, would reduce the transfer of malaria within the population. Such immunity, in addition to reducing the overall rate of malaria transmission, would, if combined with a vaccine against the asexual (disease-causing) stages, reduce the chance of selection of parasites that are resistant to the asexual vaccine by preventing their entry into the mosquito population.
Animals↗
A surface protein expressed during the transformation of zygotes of Plasmodium gallinaceum is a target of transmission-blocking antibodies.
Antibodies against gametes of malarial parasites (Plasmodium spp.) have previously been shown to block infectivity of the parasites to mosquitoes by preventing fertilization of the parasites in the insect midgut. These antibodies did not have any effect on the development of fertilized parasites. We now report that a surface protein of Mr 26,000 synthesized by zygotes of P. gallinaceum is the target of antibodies which block infectivity of the fertilized parasites to mosquitoes. Identification of this target antigen offers a new stage of the parasite against which a malaria transmission-blocking vaccine could be developed.
Aedes↗
Monoclonal antibodies against surface determinants on gametes of Plasmodium gallinaceum block transmission of malaria parasites to mosquitoes.
Monoclonal antibodies (MAb) against gametes of the chicken malaria Plasmodium gallinaceum have been derived. All reacted with the surface of extracellular gametes of the parasite in immunofluorescent antibody reactions and all agglutinated both male and female gametes. In the absence of active complement one mu isotype MAb, la 1-D5, mediated at least 95% suppression of infectivity of the parasites to Aedes aegypti mosquitoes. Individually, MAb of the gamma 1 or gamma 2a isotypes mediated only slight suppression in the absence of active complement. Certain combinations of these MAb, however, suppressed parasite infectivity by 90 to 95%. Suppression of infectivity by the MAb was shown to be mainly due to their effects on the events leading up to or including fertilization. Certain gamma 2a isotype MAb, which otherwise mediated minimal or no suppressive effect, completely abolished infectivity of the parasites if complement was present. No target antigen could be identified by immunoprecipitation of Triton X-100 extracts of surface radioiodinated zygotes or gametes of P. gallinaceum for the mu isotype MAb. All gamma isotype MAb precipitated the same three proteins of 240,000, 56,000, and 54,000 daltons under reducing conditions on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, from extracts of radioiodinated male and female gametes. These surface proteins on gametes of both sexes of P. gallinaceum thus appear to include target antigens of anti-gamete transmission blocking immunity.
Aedes↗