Disease relevance of Prkcdbp

• We have used the delayed-type hypersensitivity (DTH) response to SRBC or tuberculin to examine the role of the murine type 3 complement receptor in T lymphocyte-dependent inflammatory recruitment [1].
• Splenic and peritoneal macrophages from mice treated with Corynebacterium parvum enhanced the antibody response in vitro of normal nonadherent spleen cells to SRBC, but not to DNP-POL [2].
• The Ig borne by the six lymphomas that bind phosphatidylcholine also bind to both SRBC and bromelain-treated mouse erythrocytes [3].
• Antigen-specific responses to SRBC in vitro of B cells from all lupus strains, like those of B cells from normal strains, required a minimum of three signals (antigen, LPS, T cell-derived antigen nonspecific helper factors) [4].
• Pulmonary inflammation increased on repeated intratracheal SRBC challenge of lpr/lpr mice, in contrast to the waning response in normal mice [5].

Psychiatry related information on Prkcdbp

• The greatest depression of the response to SRBC was associated with an interval of 14 days between infection and the administration of antigen, suggesting that a particular stage of the parasite contributed significantly to immunodepression during this critical period [6].

High impact information on Prkcdbp

• Both passive transfer of cutaneous DTH to SRBC and passive transfer of the largely monocytic T cell-dependent recruitment to tuberculin in the peritoneal cavity were completely abolished by systemic 5C6 treatment [1].
• First, mice were depleted of C3 by treatment with cobra venom factor (CVF) and then immunized with SRBC with or without IgM-anti-SRBC [7].
• We have developed a plasma-free system in which washed mouse platelets lyse washed antibody and complement-sensitized SRBC targets in the presence of EDTA [8].
• These findings, as well as the fact that platelets do not lyse unsensitized innocent bystander SRBC, suggest that the complete cytotoxic system of platelets capable of specific recognition and lysis resides in their membranes [8].
• Examination of antibody responses to SRBC revealed that approximately half the normal number of indirect PFCs were observed [9].

Chemical compound and disease context of Prkcdbp

• In contrast, capsaicin-pretreated mice exhibited enhanced contact sensitivity (CS) reactions to oxazolone (greater than 90%) and DNFB (greater than 50%) and enhanced delayed-type hypersensitivity reactions to SRBC (greater than 20%) [10].
• In old NZB mice exhibiting signs of disease (splenomegaly) and in which defects in immune competence are known to occur, the injection of SRBC results in in no increase in splenic PGF2alpha levels and a decrease in cAMP levels [11].
• (3) Both pre-treatment with BCG and with cyclophosphamide (CY) augmented delayed footpad reaction in the mice immunized with SRBC in saline [12].
• The role of such suppressive T cells in the inhibitory effect exerted by Suramin on the cell-mediated delayed-type hypersensitivity response to SRBC is discussed [13].
• After intraperitoneal injection of Adriamycin, BCG or thioglycolate the ADCC of peritoneal cells toward antibody-coated SRBC was elevated to 30% in contrast to the ADCC of spleen cells [14].

Biological context of Prkcdbp

• Isolated cells were cultured for 48 h in the presence of a variety of TNP conjugates including TNP-Brucella abortus (Ba), TNP-Ficoll, TNP-sheep erythrocytes (SRBC), TNP-human gamma globulin (HGG), or TNP-ovalbumin (OVA) before being harvested and subjected to acridine orange cell cycle analysis [15].
• Inhibiting apoptosis by in vivo cyclosporine treatment prolonged lung lymphocyte accumulation following SRBC challenge [5].
• FcgammaR-mediated phagocytosis of IgG-coated SRBC was also significantly decreased in Rac2-null macrophages, as was NADPH oxidase activity in response to phorbol ester or FcgammaR stimulation [16].
• Human LDL-In is not species specific and was capable of suppressing the in vivo mouse anti-sheep erythrocyte (SRBC) hemagglutination response by 88% after the administration of 500 to 600 mug LDL-In IV, whereas human serum high density lipoproteins and fibrinogen had no effect [17].
• T helper cells from these mice, immunized to SRBC, were restricted to cooperation with B cells of the thymic H-2 haplotype [18].

Anatomical context of Prkcdbp

• Development of two distinct types of suppressor T cells was revealed in the spleen of mice after the priming with SRBC [19].
• Cultures of purified sIgA+ B cells, cloned PP Th A cells and SRBC, selectively yielded IgA antibody producers [20].
• Most of these analogue-reactive PFC preferentially lyse analogue-conjugated SRBC and cannot be detected on erythrocytes bearing the immunizing hapten [21].
• 19S helper cells in nonimmune animals were nonrosette-forming small lymphocytes; after immunization with SRBC in complete Freund's adjuvant, 19S helper cells were nonrosette-forming medium lymphocytes [22].
• In pretreated recipients, the transfer of activated B cells, but not of T cells or macrophages, resulted in an augmented production of indirect plaque-forming cells in the primary immune response to SRBC but not to horse erythrocytes [23].

Associations of Prkcdbp with chemical compounds

• Daily gastric intubation of lipopolysaccharide (LPS)-responsive C3H/HeN, BALB/c, and Swiss mice with SRBC for 2 wk resulted in oral tolerance, whereas similarly treated LPS-nonresponsive C3H/HeJ mice gave splenic anti-SRBC PFC responses, including the IgA isotype, after systemic challenge with antigen [24].
• To evaluate the mechanisms of this suppression, the in vitro antibody response to SRBC was studied using cells from cytoxan-treated mice [25].
• N-acetylmuramyl-L-alanyl-D-isoglutamine (muramyl dipeptide) stimulates in vitro primary immune responses to SRBC in T cell-depleted (nude) spleen cultures [26].
• Additional studies revealed that prior injection of BCG influencdd the ensuing magnitude of SRBC-induced trapping [27].
• Mice were immunized by i.v. injection of SRBC or by topical application of picryl chloride, and the responses were elicited by cutaneous challenge with the appropriate Ag [28].

Analytical, diagnostic and therapeutic context of Prkcdbp

• Spleen cell cultures from xid mice were unresponsive to SRBC and TI-2 antigens [29].
• C3H/HeJ mice given SRBC orally for 4 wk are not rendered tolerant to this antigen and were used as a source of PP Tcs cells for adoptive transfer to identically treated, orally tolerized C3H/HeN mice [30].
• No SRBC binding by helper cells was observed under the conditions of rosette formation used [22].
• The plaque assay, utilizing SRBC to which Staphylococcal protein A had been coupled, the developing anti-supernatant antiserum and guinea pig complement, readily detected secreting T cells [31].
• Intravenous injection of 5C6, a CR3-specific rat mAb known to impair myelomonocytic adhesion, divided the DTH to SRBC in actively immunized mice into two phases [1].

References