Recently, several unbiased approaches have identified an association between polymorphisms of the CD2 gene, and rheumatoid arthritis (RA) susceptibility.
Unlike the case in Asia and Latin America, <i>Plasmodium vivax</i> infections are rare in sub-Saharan Africa due to the absence of the Duffy blood group antigen (Duffy antigen), the only known erythrocyte receptor for the <i>P. vivax</i> merozoite invasion ligand, Duffy binding protein 1 (DBP1).However, <i>P. vivax</i> infections have been documented in Duffy-negative individuals throughout Africa, suggesting that <i>P. vivax</i> may use ligands other than DBP1 to invade Duffy-negative erythrocytes through other receptors.To identify potential <i>P. vivax</i> ligands, we compared parasite gene expression in <i>Saimiri</i> and <i>Aotus</i> monkey erythrocytes infected with <i>P. vivax</i> Salvador I (Sal I).
RH5 is a leading subunit vaccine candidate because anti-RH5 antibodies inhibit parasite growth and the interaction with its erythrocyte receptor basigin is essential for invasion.
They both share homology of domain structure, including the binding region (Region II), which consists of two homologous F1 and F2 domains and is responsible for ligand-erythrocyte receptor interaction during merozoite invasion.
The molecular mechanism(s) responsible for these host restrictions are not understood, although the interaction between the parasite blood-stage invasion ligand EBA175 and the host erythrocyte receptor Glycophorin-A (GYPA) has been implicated previously.
The protease-resistant properties of the erythrocyte receptor suggests that it is not glycophorin A or C. Additionally, analysis of mutant erythrocytes from humans has shown that EBA140 does not bind glycophorin B. Interestingly, we have identified a parasite line that lacks the eba140 gene, suggesting that this protein is not essential for in vitro invasion.
We previously demonstrated that administration of membrane glycopeptides T11 target structure (T11TS) not only rejuvenate bone marrow hematopoietic stem cells (BMHSCs) from glioma mediated hibernation by inhibiting gliomagenic overexpression of Ang-1/Tie-2 but also stimulate glioma mediated diminution of expression CD34, c-kit, and Sca-1 markers.
We present a mathematical model which describes the growth of malignant gliomas in presence of immune responses by considering the role of immunotherapeutic agent T11 target structure (T11TS).
Quantifying the role of immunotherapeutic drug T11 target structure in progression of malignant gliomas: Mathematical modeling and dynamical perspective.
Selection in G418-containing medium produced CTLLR8 transfectant clones that: (1) expressed chimeric Fc(epsilon) receptor as determined by flow cytometry; (2) bound human IgE antibodies with high affinity as determined by Scatchard analysis; (3) specifically rosetted IgE-coated SRBC; (4) lysed target cells in IgE-mediated ADCC and reverse ADCC assays; and (5) retarded tumor growth in a Winn assay.
An unusual neoplasm, best classified as a B-cell chronic lymphocytic leukemia on the basis of cytofluorographic, immunohistologic, and gene rearrangement analysis also co-expressed the T-cell associated marker CD2 (sheep erythrocyte receptor), but without other cell markers restricted to T cells.
As T11-target structure (T11TS) has documented profound immune potentiation, we aimed to investigate the role of microglia, pivotal immune cells of brain in ameliorating cryptococcosis, with T11TS immunotherapy.
In the acidic environment, WS biochars produced at low temperature were more competent than those produced at high temperature on Zn(II) and Cd(II) immobilization; while WS biochars produced at high temperature were more effective than those produced at low temperature in the alkaline environment.
We reported previously that T cells specific RORγt-transgenic-mice under human CD2 promoter (RORγt-Tg mice) developed severe spontaneous Sjögren's syndrome (SS)-like sialadenitis, induced by RORγt-overexpressing CD4<sup>+</sup> T cells and reduced regulatory T cells.