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PubMed1995

Antibodies to murine complement receptor 1 and 2 can inhibit the antibody response in vivo without inhibiting T helper cell induction.

Administration to mice of mAb against CR1/CR2 inhibits the primary and secondary in vivo Ab response. We have addressed the question of whether induction of T helper cells, in addition to B cells, is inhibited by this treatment. A hapten-carrier system was used, where one group of mice was immunized with a monoclonal CR1/CR2-specific Ab and Ag (SRBC or keyhole limpet hemocyanin (KLH)), another with Ag alone, and a third group left nonimmunized. After 2 to 15 wk, spleen cells from these mice were transferred to irradiated syngeneic recipients, together with Ag coupled to the hapten 4-hydroxy-5-iodo-3-nitro-phenacetyl (NIP). The number of NIP-specific, IgG-producing B cells, which in this system is an indication of T cell priming, was determined in an ELISPOT assay. Although the primary SRBC- or KLH-specific IgG response was inhibited markedly (74-98%) by CR1/CR2-specific Ab, no decrease in the number of NIP-specific IgG-producing B cells was detected after secondary immunization. In sharp contrast, the SRBC- or KLH-specific secondary IgG responses were low or undetectable. These findings suggest that CR1/CR2-specific Ab can inhibit the primary Ab response without affecting T helper cells and that the induction of B cell memory is decreased markedly by this treatment.

Animals↗
PubMed1994

Analysis of C3b/C3d binding sites and factor I cofactor regions within mouse complement receptors 1 and 2.

Human and murine CR1 and CR2 are defined as evolutionary homologues on the basis of their in vitro activities and a shared structural motif known as a short consensus repeat (SCR). To identify additional similarities between the two species, we analyzed the functional domains within the mouse receptors by constructing mouse-human chimeric cDNAs in which the C3 binding site of human CR2 has been replaced by different regions within the first eight SCRs of mouse CR1. Rosette analysis of cells expressing chimeric proteins, with erythrocytes bearing different mouse C3 fragments, coupled with rosette inhibition studies using specific anti-mouse CR1/CR2 mAbs reveal a weak C3b binding site within SCRs 1 and 2 of mouse CR1. There is no independent C3b interacting domain within SCRs 3 to 6, but their presence enhances C3 binding. A molecule that contains only the first six SCRs of mouse CR1 also binds C3b, but with less efficiency. There is no C3d binding area within the first six SCRs, but our data confirms previous studies indicating an additional C3b/C3d binding region within SCRs 7 and 8 of mouse CR1 (SCRs 1-2 of mouse CR2). The presence of SCRs 1 to 4 is required for C3 cofactor activity. 8C12, a mAb which blocks C3b erythrocyte rosette binding and the C3 cofactor activity of mouse CR1, binds only to chimeras containing SCRs 3 to 4.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Two functionally different follicular dendritic cells in secondary lymphoid follicles of mouse spleen, as revealed by CR1/2 and FcR gamma II-mediated immune-complex trapping.

The capacity to trap immune complexes (IC) was examined using purified peroxidase-antiperoxidase IgG on frozen sections of mouse spleen. In the absence of serum, binding of IC was confined to macrophages in the red pulp. However, when IC were applied in the presence of fresh mouse serum as a source of complement, trapping occurred on follicular dendritic cells (FDC) in the primary follicles. Trapping was specifically inhibited with monoclonal antibodies against complement receptor type 1 (CR1) (8C12) and CR 1/2 (7G6), but not with anti-CR3 (Mac-1). The binding mechanism of IC in the secondary follicles of animals immunized with sheep red blood cells differed from that observed in unimmunized mice. Here, trapping occurred both in the absence and presence of fresh mouse serum. In the absence of fresh mouse serum, trapping on FDC was mediated by FcR gamma II, as demonstrated by blocking with monoclonal antibody 2.4G2. FcR gamma II-mediated trapping was only observed on a relatively small proportion of FDC that was located in the light zone of the secondary follicles, while complement receptor-mediated IC trapping was observed in more expanding areas, including dark zone and corona. These results show that both complement receptor as well as Fc receptor can function in the binding of IC to FDC. They also provide evidence for the existence of functionally different FDC populations in the secondary lymphoid follicles of mouse spleen.

Animals↗
PubMed1993

Structure of the gene for the F allele of complement receptor type 1 and sequence of the coding region unique to the S allele.

The genes for human complement receptor type 1 (CR1) F and S alleles have been cloned and span a region of 133-160 kb on chromosome 1. The F allele was found to comprise 39 exons and the S allele contains an additional 8 exons. The leader sequence and 5'-untranslated region are contained in one exon. Each of the long homologous repeats (LHR), which contain seven short consensus repeats (SCR), is composed of 8 exons. Within a LHR, SCR 1, 5, and 7 are each encoded by a single exon, SCR 2 and 6 are each encoded by 2 exons, and a single exon codes for SCR 3 and 4. The transmembrane region is encoded by 2 exons and the cytoplasmic domain and the 3'-untranslated regions are coded for by separate exons. The sequences of the eight S allele-specific exons were very similar to those from LHR-A and -B, as was predicted by comparison of the genomic restriction maps. It had previously been suggested that the alleles of CR1 have arisen by a mechanism of unequal crossover. A comparison of intron sequences from LHR-A, -B, -C, and -S revealed data that support this hypothesis. The homologies of intron sequences from LHR-A, -B, and -C indicated that the crossover event between LHR-A and -C that gave rise to LHR-B probably occurred within the fourth exon of these LHR. Likewise, the crossover event between LHR-A and -B that produced LHR-S probably occurred within a 383 bp region around the sixth exon. Analysis of RNA from peripheral blood cells by the S1 nuclease assay indicated that the transcription start site is 111 bp upstream of the translation initiation codon ATG. The 5' rapid amplification of cDNA ends confirmed this position as a transcription start site and revealed another possible start site 29 bp further upstream.

Alleles↗
PubMed1993

Herpes simplex virus glycoprotein C: molecular mimicry of complement regulatory proteins by a viral protein.

Herpes simplex virus (HSV) encodes a protein, glycoprotein C (gC), which binds to the third complement component, the central mediator of complement activation. In this study the structural and functional relationships of gC from HSV type 1 (HSV-1) and known human complement regulatory proteins factor H, properdin, factor B, complement receptor 1 (CR1) and 2 (CR2) were investigated. The interaction of gC with C3b was studied using purified complement components, synthetic peptides, antisera against different C3 fragments and anti-C3 monoclonal antibodies (mAb) with known inhibitory effects on C3-ligand interactions. All the mAb that inhibited gC/C3b interactions, in a differential manner, also prevented binding of C3 fragments to factors H, B, CR1 or CR2. No blocking was observed with synthetic peptides representing different C3 regions or with factor B and C3d, whereas C3b, C3c and factor H were inhibitory, as well as purified gC. There was no binding of gC to cobra venom factor (CVF), a C3c-like fragment derived from cobra gland. Purified gC bound to iC3, iC3b and C3c, but failed to bind to C3d. Glycoprotein C bound only weakly to iC3 derived from bovine and porcine plasma, thus indicating a preference of the viral protein for the appropriate host. Binding of gC was also observed to proteolytic C3 fragments, especially to the beta-chain, thus suggesting the importance of the C3 region as a binding site. Purified gC from HSV-1, but not HSV-2, inhibited the binding of factor H and properdin but not of CR1 to C3b. The binding of iC3b to CR2, a molecule involved in B-cell activation and binding of the Epstein-Barr virus, was also inhibited by the HSV-1 protein. As factor H and properdin, the binding of which was inhibited by gC, are important regulators of the alternative complement pathway, these data further support a role of gC in the evasion of HSV from a major first-line host defence mechanism, i.e. the complement system. In addition, the inhibition of the C3/CR2 interaction may suggest a possible immunoregulatory role of HSV glycoprotein C.

Antibodies, Monoclonal↗
PubMed1996

Identification and characterization of complement C3 receptors on human astrocytes.

Astrocytes express C components and have been implicated as a major source of intrathecal C. To ascertain the effects of C activation on these cells, we have evaluated the expression of CR1, CR2, and CR3 (CD35, CD21, and CD11b/CD18) in primary fetal astrocytes and astrocyte cell lines. None of the astrocyte cells tested expressed CR3, whereas primary astrocytes and one of four astrocyte cell lines expressed CR1 (220 kDa), as assessed at the protein and mRNA level. Primary fetal astrocytes and all four astrocyte cell lines expressed CR2 (155 kDa). Expression of CR2 by astrocytes was confirmed at mRNA level by reverse-transcriptase PCR, using different combinations of seven specific CR2 oligonucleotides, and by partial sequencing of the astrocyte CR2 cDNA. Astrocyte CR2 cDNA presented 100% homology with the lymphocyte CR2 cDNA between the position 181 bp to 600 bp and position 1017 bp to 1347 bp. An alternative splicing pattern of exon 11, reported previously in B cells, was observed in astrocyte CR2 cDNA. Astrocyte CR2 was functional, in that it specifically bound C3d and the EBV surface protein gp340, and the binding was blocked specifically with polyclonal anti-CR2. Scatchard analysis of membrane expression of CR2 on astrocytes revealed 2000 functional sites per cell with a Kd (3 x 10(-7) M) identical with that of CR2 on B cell (Raji).

Astrocytes↗
PubMed1997

The role of follicular and interdigitating dendritic cells in HIV-related lymphoid hyperplasia: localization of fascin.

Fascin is a 55-kDa, actin-bundling protein expressed in follicular and interdigitating dendritic cells (DCs). Because these cells play a pivotal role in the pathogenesis of human immunodeficiency virus-related lymphoid hyperplasias (HLP), we evaluated them in 49 cases by immunohistochemical localization of fascin, and we related the findings to the histologic stage of disease. Fifteen cases of early HLP revealed strong localization of fascin within DCs of hyperplastic follicles and intense staining in interdigitating DCs and their processes in the interfollicular zones. Some follicles revealed focal disruption of the fascin-positive dendritic framework. DCs were also aligned beneath the peripheral sinuses of the node. In 15 cases of progressive HLP with partial follicular involution, 3 cases revealed findings similar to those described above. Twelve cases revealed loss of follicular dendritic staining, which was moderate in five cases and marked in seven. Residual clusters of DCs remained after partial dissolution. Interfollicular dendritic staining was reduced in 13 cases, and perisinusoidal staining was reduced in 7. In late-stage HLP, staining of both follicular and interdigitating DCs was reduced or absent. Nine cases of diffuse immunoblastic or angioimmunoblastic lymphadenopathy-like proliferation had markedly reduced or absent follicular DCs, but prominent staining was present in interfollicular DCs, which formed a meshwork throughout the node in eight cases. Two cases of hyaline-vascular lymphoid hyperplasia had increased follicular DCs forming a tight syncytial network. In most cases, there was reduction of dendritic fascin-expressing cells with advanced disease and destruction of the dendritic framework of the node. Diffuse hyperplasia of fascin-positive interdigitating cells occurred in cases with angioimmunoblastic morphologic features, and cases of hyaline-vascular lymphoid hyperplasia had increased follicular dendritic histiocytes forming a tight syncytial network. Destruction of DCs and, in some cases, interdigitating cell hyperplasia might be associated with the variable clinical course of HLP.

Biopsy↗
PubMed1997

Mouse complement receptors type 1 (CR1;CD35) and type 2 (CR2;CD21): expression on normal B cell subpopulations and decreased levels during the development of autoimmunity in MRL/lpr mice.

Human complement receptors type 1 (hCR1;CD35) and type 2 (hCR2;CD21) are expressed on B lymphocytes at specific stages during differentiation and activation. These receptors play critical roles in the immune response to T-dependent Ags in addition to germinal center formation. Expression of both hCR2 and hCR1 is decreased on B lymphocytes of patients with systemic lupus erythematosus (SLE). We have studied the expression of mouse CR2 and CR1 on normal populations of mouse B lymphocytes in BALB/c mice. Our results demonstrate that expression of these receptors in the normal state closely parallels that of hCR2. During bone marrow development, expression is first detected on low B220/high IgM cells, demonstrating that complement receptors appear after central tolerance mechanisms are completed. In the splenic microenvironment the highest levels of receptor expression are found on marginal zone B lymphocytes. Mouse CR2 and CR1 are also found on peritoneal B1a and B1b cells in addition to IgA+ Peyer's patch B cells. Activation of splenic B cells under Th2 conditions results in a marked decrease in receptor expression. To determine whether the patterns of receptor expression also parallel those found in human disease, we studied the MRL lpr/lpr (MRL/lpr) model of SLE. Interestingly, we found an early decrease in complement receptor expression that is progressive and first detectable before major clinical manifestations of nephritis. We hypothesize that the early decrease in complement receptor expression such as that demonstrated by MRL/lpr mice plays an important role in the pathogenesis of murine and perhaps human SLE.

Animals↗
PubMed1997

Characterization of C3-binding proteins on mouse neutrophils and platelets.

In the mouse, MCR1 and MCR2 on B lymphocytes are encoded by alternatively spliced Cr2 gene transcripts. Immune adherence receptors that bind C3 are present on mouse platelets and unstimulated neutrophils, yet they are not MCR1 or MCR2. To examine C3b- and C3d-binding proteins on mouse platelets and neutrophils, we performed C3b and C3d affinity chromatography as well as immunoprecipitation studies using previously described Ab to MCR1/MCR2 (mAb clones 8C12, 7G6, and 7E9 and polyclonal Ab BRN-1). Mouse neutrophils contained a 190-kDa membrane protein that specifically bound to C3b-Sepharose. Preabsorption of neutrophil proteins with anti-MCR1/MCR2 Ab did not affect the recovery of the 190-kDa C3b-binding protein by subsequent C3b affinity chromatography. Thus, this protein is immunologically distinct from the previously described MCR1 and MCR2 proteins. By virtue of its size and C3b-binding capacity, the 190-kDa protein was named C3bR-190. C3bR-190 was also apparent on platelets, but in reduced amounts. BRN-1 anti-MCR1/MCR2 Ab immunoprecipitated proteins of 125 and 150 kDa from surface-radiolabeled mouse platelets, which specifically bound to C3d-Sepharose. However, these proteins were not identified by mAb to MCR2, thus distinguishing them from previously described MCR2. These proteins were named C3dR-125 and C3dR-150. Therefore, we have identified a 190-kDa C3b-binding protein on mouse neutrophils and 125- and 150-kDa C3d-binding proteins on mouse platelets. These appear to be distinct from the heretofore identified mouse B lymphocyte MCR1 and MCR2. The identity of these C3b- and C3d-binding proteins on mouse neutrophils and platelets awaits further study.

Animals↗
PubMed1998

Cross-linking CD21/CD35 or CD19 increases both B7-1 and B7-2 expression on murine splenic B cells.

Activation of the complement cascade and ligation of complement C3 receptors on B cells represent an important bridge between innate and Ag-specific acquired immunity. We show here that cross-linking of mouse CD21 (complement receptor type 2, CR2, C3d receptor) and CD35 (complement receptor type 1, CR1, C3b/C4b receptor) or co-cross-linking of CD21/CD35 and surface IgM rapidly up-regulates both B7-1 and B7-2 expression on murine resting splenic B cells. CD21/CD35-mediated up-regulation of both B7-1 and B7-2 expression is observed within 14 h, while other stimuli up-regulate only B7-2 but not B7-1 at this early time point. Consistent with the increase in B7 levels, BALB/c B cells on which surface IgM and CD21/CD35 have been co-cross-linked stimulate C57BL/6 T cells more effectively than controls. This CD21/CD35-enhanced allogeneic MLR is blocked nearly completely by anti-B7-2 mAbs and partially by anti-B7-1 mAbs. In addition, cross-linking of CD19, which is physically associated with CD21/CD35, leads to increased B7-1 and B7-2 expression. These data suggest that CD21/CD35 ligation results in enhanced B cell Ag presentation using costimulatory mechanisms shared with other activators and thus works cooperatively in this process. Rapid up-regulation of B7-1 expression, a unique response to CD21/CD35 and CD19 cross-linking, may be a particularly important effect of C3-containing ligands. We propose that CD21/CD35- and CD19-mediated B7-1 and B7-2 up-regulation is an important mechanism by which complement activation links innate and acquired immunity.

Animals↗
PubMed1998

Microvillous lymphomas are B-cell neoplasms that frequently express CD56.

Microvillous lymphomas (MVLs) are rare, poorly defined, large transformed cell lymphomas characterized by a cohesive sinus growth pattern and ultrastructural cytoplasmic processes. Most MVLs express B-cell antigens and have been compared ultrastructurally to transformed follicular center cells and follicular dendritic cells. For additional definition of the immunophenotype of these unusual B-cell lymphomas, we evaluated eight cases of MVL for B-cell-associated antigens (CD21, CD35, CDw75, DBA.44, bcl-2) using paraffin immunoperoxidase. CD56, the neural cell adhesion molecule, was tested because of the unusual, cohesive, sinus pattern of tumor cell growth seen in MVL. Molecular analysis for immunoglobulin heavy chain and bcl-2 gene rearrangements was performed to confirm B-cell clonality and to evaluate cases for possible follicular origin. All of the cases were marked as B cells (CD20 positive), and the clonal nature confirmed by immunoperoxidase in five cases (63%) of eight and polymerase chain reaction for immunoglobulin heavy chain in seven cases (88%) of eight. CDw75 staining was present in six cases and CD74 in seven. DBA.44 and CD21 and CD35 were negative in all of the cases, and four cases (50%) of eight expressed CD56. bcl-2 protein expression was seen in seven of eight cases; bcl-2 gene rearrangement was present in one case (33%) of three studied. In conclusion, MVLs are B-cell lymphomas demonstrating clonal immunoglobulin heavy chain gene rearrangement. The neoplastic cells express CDw75 and bcl-2 protein. The presence of bcl-2 rearrangements in a limited number of cases implies that at least some MVLs have a follicular origin. Fifty percent of MVLs express CD56, suggesting a role for adhesion molecules in the distribution of this lymphoma.

Aged↗
PubMed1998

Alterations in fascin-expressing germinal center dendritic cells in neoplastic follicles of B-cell lymphomas.

Germinal center dendritic cells (GCDCs) have essential functions in retention of immune complexes within secondary follicles, B-lymphocyte antigenic stimulation, B-cell activation, homing of B-cells via adhesion molecules such as ICAM-1 and VCAM-1, and B-cell survival via apoptosis. The neoplastic cells of follicular lymphomas (FLs) are thought to derive from follicular B lymphocytes, but their relationship to GCDCs remains unclear. This study used immunohistochemical staining for fascin, a 55-kDa actin-bundling protein strongly expressed in GCDCs and their processes, to evaluate their distribution in neoplastic follicles. Forty-two cases of B-cell FL were evaluated, and immunoreactive staining for fascin was compared with six cases of Castleman's disease (CD) and six cases of follicular hyperplasia. FLs generally revealed decreased or absent fascin-staining GCDCs, suggesting loss of fascin expression by dendritic cells in neoplastic follicles compared with hyperplastic follicular centers. In some follicles, there was partial retention of dendritic architecture with islands of residual syncytial network. Interdigitating reticulum cells in the parafollicular regions revealed normal fascin expression with intense staining of dendritic processes. In contrast with FLs, cases of follicular hyperplasia revealed normal or increased fascin-positive follicular dendritic cells, and in cases of hyaline vascular CD, follicular dendritic cells revealed tight syncytial networks. These results suggest that GCDCs are deficient in neoplastic follicles, compared with benign reactive or hyperplastic follicles. This alterations in the germinal center microenvironment might explain the inability of FL cells to present antigen to T lymphocytes and to mount an effective antitumor immune response.

Carrier Proteins↗
PubMed1998

Expression of complement receptors 1 and 2 on follicular dendritic cells is necessary for the generation of a strong antigen-specific IgG response.

Two mechanisms could account for the impaired humoral immune response found in Cr2-/- mice. The absence of complement receptors 1 and 2 (CR1, CR2) on B cells could affect their activation. Alternatively, impaired Ag trapping by follicular dendritic cells (FDC) could affect B cell maturation into Ig-secreting or memory B cells. To compare the roles of CR1 and CR2 on B cells vs FDC in this abnormal response, bone marrow (BM) chimeric mice were generated and immunized with specific T-dependent Ags. The primary and secondary Ab response was measured. Cr2+/+ animals reconstituted with a Cr2-/- BM generated a diminished but detectable humoral immune response compared with controls. When injected with preformed immune complexes (IC), these mice maintained follicular IC localization. Cr2-/- animals reconstituted with a Cr2+/+ BM had an initial rise in the Ab titer, but were unable to maintain it as shown by a pronounced decrease in the IgG titer. This defect persisted during the secondary immune response. Follicular IC trapping was also impaired. Despite the abnormal Ab response, germinal center formation was retained in all of the chimeric animals. These experiments are the first to demonstrate an absolute requirement for CR1 and CR2 expression on FDC in the generation of a normal humoral immune response.

Animals↗
PubMed1998

Complement opsonization is required for presentation of immune complexes by resting peripheral blood B cells.

Complement receptor 2 (CD21, CR2) is a B cell receptor for complement degradation products bound to Ag or immune complexes. The role of CD21 in mediating Ag presentation of soluble immune complexes by resting B cells was studied. Complement-coated immune complexes were formed by the incubation of influenza virus with serum from immune donors. These complexes bound to peripheral blood B cells in a complement-dependent manner. The binding required CD21 or, to a lesser extent, complement receptor 1 (CR1, CD35). B cells pulsed with immune complexes containing complement elicited a response from a panel of influenza-specific T cell clones, while those pulsed with immune complexes formed in the absence of complement did not. The expression of the early activation marker CD69 and the costimulatory molecule CD86 were not induced by CD21 ligation alone, suggesting that CD21-mediated Ag presentation occurs independently of B cell activation. Up-regulation of these markers required exposure to T cell factors elicited by the recognition of Ag derived from complement-containing immune complexes. These findings suggest that binding of Ag to CD21 enables Ag-nonspecific B cells to participate in the activation of Ag-specific T cells in a process that occurs independently of well-characterized B cell activation events.

Antigen Presentation↗
PubMed1991

Flow cytometric assay for phagocytosis of human monocytes mediated via Fc gamma-receptors and complement receptor CR1 (CD35).

We developed a simple flow cytometric assay for phagocytosis by human monocytes that is mediated via Fc gamma receptors and the complement receptor CR1 (CD35), using fluorescent latex beads carrying IgG and complement components C4b and C3b. To prepare fluorescent latex beads carrying IgG(BA), BSA-coated latex beads (B) were incubated with diluted rabbit anti-BSA IgG. To bind complement components, BA-particles were incubated with whole human serum pretreated with K-76 monocarboxylic acid (K-76COOH). K-76COOH inhibits the activities of C5 and factor I (12,13), resulting in the deposition of C1,4b,2a,3b on BA-particles (BAC1,4b,2a,3b). Further incubation of BAC1,4b,2a,3b with EDTA-GVB at 37 degrees C gave particles carrying IgG and C4b,C3b (BAC4b,3b). The C3 fragment, C3b, was confirmed to present on BAC1,4a,2a,3b particles by SDS-PAGE and immunoblot, and these particles were calculated to have approximately 25,000-30,000 C3b molecules per particle. To evaluate the particle attachment, the phagocytic assay was performed with 3 microM cytochalasin D treated cells. The percent cells with ingested particles and the number of ingested particles/100 cells for 60 min were estimated, being 5.1% and 5.4 for B, 12.3% and 26.7 for BA, 42.5% and 108.7 for BAC4b,3b, and 42.6% and 112.5 for BAC1,4b,2a,3b, respectively.

Antigens, Differentiation↗
PubMed2000

Microglial and astrocytic reactions prior to onset of thalamic cell death after traumatic lesion of the rat sensorimotor cortex.

The temporospatial relationship between microglial and astrocytic reactions and delayed thalamic cell death was examined 1-7 days following a traumatic cold lesion of the rat sensorimotor cortex using immunocytochemistry in combination with terminal deoxynucleotidyltransferase-mediated biotinylated dUTP nick end labeling (TUNEL) of nuclear DNA fragmentation. No or only occasional TUNEL-positive cells were found in the thalamic relay nuclei up to 3 days after trauma. After 7 days, on the other hand, a considerable number of TUNEL-positive cells were seen in the ventrobasal, the ventrolateral and posterior thalamic nuclei. Already 3 days after trauma, i.e., before cell injury was detectable, many protoplasmic astrocytes, which were reactive for glial fibrillary acidic protein, and ramified microglia, which were positive for complement receptor type 3b (CR3b) but negative for major histocompatibility complex (MHC) class II antigen, were noticed in the thalamus. The number of labeled astro- and microglia further increased after 7 days, when DNA fragmentation became evident. At this time, the morphology of microglia shifted towards bushy and rod-like cells, and microglia became also reactive for MHC class II antigen. Clusters of CR3b- and MHC class II-positive microglia were found in the ventrobasal thalamus. The present findings demonstrate that trauma-induced microglial and astrocytic reactions appear in the thalamus prior the onset of cell damage.

Animals↗
PubMed1995

[Effect of yishen jianpi drugs on T lymphocyte subsets, soluble interleukin-2 receptor and red blood cell immunity of senile deficiency syndrome patients].

UNLABELLED: To evaluate the effect of Yishen Jianpi drugs (YJD) on immunological function of the Senile Deficiency Syndrome (SDS) patients, T lymphocyte subsets, soluble interleukin-2 receptor (SIL-2 R), the red blood cell immunity, the rate of red blood cell C 3b receptor rosette (RBC-C 3 bRR) and red blood cell immune complex rosette (RBC-ICR) were dynamically investigated in 31 SDS patients as well as in normal controls. RESULTS: the percentage of CD3, CD4 and CD4/CD8 ratio and the rate of RBC-C 3 bRR in SDS were all significantly lower than that of control (P < 0.01). The further analysis also revealed that between the immunological indices of CD4/CD8 ratio and SIL-2 R in SDS patients were markedly negative correlated (r = -0.572, P < 0.01) while positive correlated (r = 0.435, P < 0.02) markedly between CD4/CD8 and RBC-C 3 bRR. After treatment with YJD, in comparing pretreatmentally, all the above-mentioned immunological indices, following the relief of clinical manifestation of SDS, they were corresponding negatively changed, and there were marked significance (P < 0.01) except red blood cell immunity. It suggested that YJD would markedly improve and/or regulate immunological function in SDS.

Aged↗