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PubMedDate not supplied

Ripley-like anti-Rh associated with red blood cell-bound IgG aggregates.

A commercial Rho (D) immune globulin after heating at 63 C became Ripley-like in the Rh-positive red blood cells coated with this heated globulin carried biologic activities similar to those of red blood cells coated with Ripley anti-CD serum. These coated red blood cells fixed complement and were agglutinated by all 20 sera containing rheumatoid factor (RF). The RF-Rh-hemagglutinations were more readily inhibited by heated than by unheated human IgG. The heated globulin had no such effect on Rh-negative red blood cells. Fractionation studies by Na2SO4 precipitation and/or Sephadex G-200 gel filtration revealed that heat-induced IgG aggregates in heated globulin were responsible for the biological activities. In contrast, these activities in Ripley serum were carried by IgG monomers. Another anti-CD serum (Heyman), tested in paralledl, was found to be indistinguishable from Ripley. a pooled RF serum, after multiple adsorptions with red blood cells coated with globulin, lost its agglutination activity to red blood cells coated with Ripley or Heyman serum.

Chemical Precipitation↗
PubMed1979

Shared idiotypic determinants on antibodies and T-cell-derived suppressor factor specific for the random terpolymer L-glutamic acid60-L-alanine30-L-tyrosine10.

T-cell derived suppressor factors (TsF) specific for the random copolymers L-glutamic acid60-L-alanine30-Ltyrosine10 and L-glutamic acid60-L-alanine40, referred to as GAT and GA, respectively, were prepared and partially purified on the approprate antigen immunoadsorbents. GAT-TsF obtained from nonresponder DBA/1 (H-2q) and SJL (H-2s) mice were passed over immunoadsorbents prepared from normal guinea pig serum (NGPS) or guinea pig anti-idiotype antiserum (anti-CGAT) specific for a common cross-reactive idiotype found on most anti-GAT antibodies in all mouse strains tested. Both the directly suppressive activity of the GAT-TsF and the ability of GAT-TsF to induce new suppressor T cells (Ts2) in vitro were adsorbed to and fully recoverable from the guinea pig anti-CGAT-Sepharose immunoadsorbent, while the TsF passed through the control NGPS-Sepharose without appreciable binding. The SJL GAT-TsF specifically eluted from anti-CGAT-immunoadsrobents was shown to still posses I-J determinants. These data provide evidence suggesting a sharing of V region structures between B-cell antibody and T-cell suppressor factor specific for an antigen (GAT) under Ir gene control, in agreement with earlier studies on T and B-cell alloreceptors, T-cell helper factors, and T and B-cell receptors for conventional antigens.

Alanine↗
PubMed1979

Tolerance induction during ontogeny. I. Presence of active suppression in mice rendered tolerant to human gamma-globulin in utero correlates with the breakdown of the tolerant state.

A specific state of T- and B-cell tolerance to human gamma-globulin (HGG) was induced in utero by intravenous administration of the deaggregated antigen to pregnant BALB/cCr mice. Tolerance persisted in the offspring until the 12th-wk of age and then began to gradually disappear. Suppressor cells could only be found when responsiveness to HGG ultimately appeared in the in utero-treated animals but not when they were completely unresponsives. In contrast, HGG-specific suppressors found in animals made unresponsive to HGG as adults appear to be associated with either the establishment and/or maintenance of the unresponsive state. To the extent that these experiments are consistent with natural self-tolerance to a serum protein, we conclude that active suppression is not a prerequisite from maintenance of unresponsiveness to self.

Animals↗
PubMed1979

Functional analysis of T cells expressing Ia antigens. I. Demonstration of helper T-cell heterogeneity.

We have examined the expression of I-region antigens on functional subpopulations of murine T cells. A.TH anti-A.TL (anti-Ik, Sk, Gk) alloantiserum was raised by immunization of recipients with concanavalin A (Con A) stimulated thymic and peripheral T-cell blasts. In contrast to similar antisera made by conventional methods, the anti-Ia blast serum was highly cytotoxic for purified T lymphocytes. Moreover, it reacted in a specific fashion with T cells having particular functions. Treatment of keyhole limpet hemocyanin (KLH)-primed B10.A (H-2 alpha) T cells with this antiserum plus complement resulted in the elimination of helper activity for B-cell responses to trinitrophenyl-KLH. Inhibition was shown to be a result of the selective killing of one type of helper T cell whose activity could be replaced by a factor(s) found in the supernate of Con A-activated spleen cells. A second type of helper cell required for responses to protein-bound antigens appeared to be Ia-. By absorption and analysis on H-2 recombinants, at least two specificities were detectable on helper T cells; one mapping in the I-A subregion and a second in a region(s) to the right of I-J. In addition, the helper T cell(s) involved in the generation of alloreactive cytotoxic lymphocytes was shown to be Ia+, whereas cytotoxic effector cells and their precursors were Ia- with this antiserum. These results provide strong evidence for the selective expression of I-region determinants on T-cell subsets and suggest that T-cell-associated Ia antigens may play an important role in T-lymphocyte function.

Animals↗
PubMed2025

Continuous DNA Methylation Deconvolution-Based Surrogate for B-Cell Differentiation State in CLL.

Chronic Lymphocytic Leukemia (CLL) is clinically divided into IGHV mutated (M-CLL) and IGHV unmutated (U-CLL) subtypes, which are thought to arise from distinct cells of origin along the B-cell differentiation pathway. We measured genome-scale DNA methylation in purified CLL samples ( n = 89) and utilized reference-based cell deconvolution techniques to develop a continuous metric of epigenetic similarity across a B-naive-like to B-memory-like scale (B-Index). B-Index accurately classifies CLL into clinical subtypes (98.8%), has a stronger epigenetic signal than IGHV gene percent identity, and demonstrates additional epigenetic signal within the M-CLL subgroup. We demonstrate that U-CLL is epigenetically more similar to B-memory than B-naive cells and reconcile previous reports of a B-naive-like epigenetic signal. The B-memory-like program of U-CLL is enriched for binding sites of transcription factors related to the germinal center activation pathway. Our findings provide epigenetic evidence for discerning CLL mechanisms of initiation and cell of origin. We also identified an epigenetic signal associated with tumor burden, which may have some relation to viral infections such as Epstein-Barr-Virus. Our cell-type deconvolution-based approach to developing a continuous metric for CLL epigenetic differentiation state can be applied to other tumors with multiple subtypes across differentiation stages.

B-memory-like↗
PubMed1977

Suppression of immunological activities by mouse amniotic fluid.

Mouse amniotic fluid (MAF) was shown to be capable of suppressing those antibody responses observed in euthymic or athymic mouse spleen cell cultures to the T-independent antigens dinitrophenylated Ficoll (DNP-Ficoll) and trinitrophenylated lipopolysaccharide (TNP-LPS) and to the polyclonal B-cell activators LPS and purified protein derivative of tuberculin (PPD). Titration experiments demonstrated that the suppressive capacity of MAF for either LPS or DNP-Ficoll responses was maintained up to a MAF dilution of 1:120. Preincubation of spleen cells obtained from athymic mice with MAF for 8 h significantly suppressed polyclonal B-cell activation of such cells induced by LPS, although suppression was greater when MAF was present during the entire culture period. In addition, the suppressive activity that MAF demonstrated for antibody production induced by DNP-Ficoll or LPS was not lost as a result of dialysis. MAF also suppressed the secondary in vitro proliferative responses of lymph node cells sensitized to the T-dependent antigen human gamma globulin (HGG). HGG-induced proliferation of such cells appeared to be more susceptible to suppression effected by MAF than concanavalin-A-induced proliferation.

Amniotic Fluid↗
PubMed1979

The immunopathogenesis of progressive chronic inflammatory periodontal disease.

Natural, humoral and cellular immune mechanisms have all been implicated in the pathogenesis of chronic inflammatory periodontal disease. However, confusion still exists as to the role played by each of these immunological mechanisms. Recently, characterization of the cell types within the progressive lesion has been established, in which four recognizable zones were described. Immediately subjacent to the epithelium lining the periodontal pocket both polymorphonuclear leukocytes (PMN's) and macrophages were seen, while cells deeper in the tissues had the morphological appearance of lymphocytes. The majority of these lymphocytes had a B-cell phenotype although a few T-cells and macrophages were found. On the advancing front of the lesion the cells had the morphological appearance of plasma cells, the majority of which contained IgG. Other cells found in this region had the morphology of plasma cells yet contained no cytoplasmic immunoglobulin, but they did contain substantial amounts of lysosomal enzymes. Similar cells have previously been described in periodontal disease; their frequent association with fibroblasts may suggest that they are important in the pathogenesis. Deposits of IgG and fibrin were found in the fibrous tissue band surrounding the lesion. These results are reviewed and, although the zones described were not anatomically distinct, by describing the lesion in this way it was possible to establish a convenient model to explain the immunopathogenesis of progressive chronic inflammatory periodontal disease. In this respect, progressive chronic inflammatory periodontal disease in man should be considered as a B-cell lesion.

Animals↗
PubMed1979

A rapid technique for measuring calcium uptake in mitogen-induced T and B lymphocytes.

The procedures for lymphocyte activation and for removing the cells from the radioactive loading solution in incubation medium were modified to routinely obtain significant and reproducible 45Ca2+ uptakes in mitogen-induced mouse T and B lymphocytes. Factors such as mouse strain, lymphocyte origin, and media pH were not critical to the 45Ca2+ uptake measurements. In contrast, factors such as lymphocyte cell concentration during mitogenic activation, filtering the 45Ca2+:3H2O mixtures, and the nature and purity of the B-cell mitogens were critical for obtaining maximal and reproducible 45Ca2+ uptakes. Centrifugation through silicone oil into sucrose was an efficient and rapid procedure for separating the cells from the radioactive loading solution in the incubation medium. Using optimal conditions, an approximate twofold increase in 45Ca2+ uptake (representing an influx of approximately 97 amol per lymphocyte and an increase in average cellular Ca2+ of approximately 0.72 mM) was routinely obtained with purified mouse lymphocytes activated with a variety of T- and B-cell mitogens (using concentrations resulting in maximal [3H]thymidine incorporation). A larger 45Ca2+ uptake was routinely obtained with mitogenic concentrations of A23187, a divalent cation ionophore stimulating T cells. Experiments employing [14C]sucrose and [14C]inulin with control and mitogen-induced lymphocytes showed that the trapped extracellular fluid measurements in the cell pellets should be used to correct the magnitude of the 45Ca2+ uptake measurements.

Animals↗
PubMed2026

BCL11B enhancer hijacking by t(14;16)(q32;q24) translocation defines a novel high-risk subtype of T-ALL.

The molecular classification of T-cell acute lymphoblastic leukemia (T-ALL) remains incomplete, limiting risk stratification and the development of targeted therapies. Enhancer hijacking is a critical oncogenic mechanism that deregulates proto-oncogenes by repositioning cisregulatory regions via structural variants. Here, we performed an integrated analysis of pediatric and adult T-ALL and mixed-phenotype acute leukemias (MPALs), using whole-genome and whole-transcriptome sequencing. This analysis identified a group of 14 patients with predominantly T-lineage neoplasms driven by a t(14;16)(q32;q24) translocation, harboring universal GATA3 mutations and CDKN2A/B deletions. Mechanistically, this translocation repositions the ThymoD locus downstream of BCL11B, causing monoallelic, ectopic overexpression of FENDRR and mesenchymal transcription factor genes FOXF1 and FOXC2 and activating epithelial-mesenchymal transition transcription signatures. Immunophenotypic and single-cell RNA sequencing analyses revealed marked lineage ambiguity with myeloid and B-cell differentiation potentials specific to this subtype. Furthermore, functional analyses in CD34+ cord blood cells demonstrated that FOXF1 overexpression promotes myeloid differentiation while suppressing T-cell differentiation, serving as a key factor for lineage specification. Clinically, this subtype was detected in 0.15% to 4.0% of T-ALL/MPAL cases depending on the cohort, showing a median age of 15 years and enrichment in adolescents and young adults. Importantly, patients with t(14;16)(q32;q24) have an extremely poor prognosis, showing a trend toward worse outcomes than high-risk groups such as KMT2A-rearranged early T-cell progenitor-like, SPI1-rearranged, and LMO2 γδ-like T-ALLs. The unique molecular landscape and poor prognosis of patients with the t(14;16)(q32;q24) translocation underscore the need for the development of novel subtype-specific therapeutic approaches.

Humans↗
PubMed2025

Network pharmacology approach to unveiling the mechanism of berberine in the amelioration of morphine tolerance.

OBJECTIVE: To investigate the mechanism underlying the effect of the Huanglian decoction (, HLD) on morphine tolerance (MT), using network pharmacology, and to verify these mechanisms in vitro and in vivo. METHODS: Available biological data on each drug in the HLD were retrieved from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform. The target proteins of MT were retrieved from the GeneCards, PharmGkb, Therapeutic Target Database, DrugBank, and Online Mendelian Inheritance in Man databases. Information regarding MT and the drug targets was compared to obtain overlapping elements. This information was imported into the Search Tool for the Retrieval of Interacting Genes/Proteins platform to obtain a protein-protein interaction network diagram. Then, a "component-target" network diagram was constructed using screened drug components and target information, viaCytoscape (Institute for Systems Biology, Seattle, WA, USA). The database for annotation, visualization, and integrated discovery was used for Gene Ontology enrichment and Kyoto Encyclopedia of Genes and Genomes pathways analyses. Pathway information predicted by network pharmacology was verified using animal studies and cell experiments. RESULTS: Network pharmacology analysis identified 22 active compounds of HLD and revealed that HLD partially ameliorated MT by modulating inflammatory, apoptosis, and nuclear factor kappa B (NF-κB) signaling pathways. Berberine (BBR), one of the main components of HLD, inhibited the development of MT in mice. BBR reduced cell viability while increasing B-cell lymphoma 2 (Bcl-2) protein expression and decreasing CD86, NF-κB, Bax, and Caspase-3 protein expression in brain vascular 2 (BV2) mcroglia cells treated with morphine. Additionally, BBR contributed to a reduction in pro-inflammatory cytokine release and apoptotic cell number. CONCLUSIONS: BBR, a key component of HLD, effectively suppressed microglial activation and neuro-inflammation by regulating the NF-κB and apoptosis signaling pathways, thereby delaying MT. This study offers a novel approach to enhance the clinical analgesic efficacy of morphine.

Berberine↗
PubMed2026

RAG-mediated structural variation and its impact on relapse risk in acute lymphoblastic leukemia.

Relapse during treatment of B-cell acute lymphoblastic leukemia (B-ALL) is a harbinger of poor outcomes. Identifying biomarkers for subsequent relapse risk which are detectable at B-ALL diagnosis remains a priority. Off-target recombination-activating gene (RAG)-mediated structural variants (SVs) generate genomic instability that drives leukemogenesis and may underlie treatment resistance. Leveraging sequencing data in 1,496 pediatric B-ALL patients enriched for relapse status (relapse n=532; non-relapse n=964), we characterized RAG-mediated SVs across B-ALL molecular subtypes and examined their association with patient characteristics and their impact on clinical outcomes. Off-target RAG-mediated SVs were overall frequent, particularly in ETV6::RUNX1, ETV6::RUNX1-like, and Ph-like B-ALL subtypes, while increasing age-at-diagnosis was positively associated with burden of off-target RAG-mediated SVs (P<.001). Off-target RAG-mediated SVs with a recombination signal sequence (RSS) at one breakpoint, a hallmark of off-target RAG activity, were significantly more frequent at diagnosis in patients who subsequently relapsed (P=.001). This association remained significant in multivariable regression analysis (per SV odds ratio [OR]:1.08, 95%CI:1.04-1.12), in minimal residual disease (MRD)-negative patients (OR:1.09, 95%CI:1.04-1.14) and across subtypes. Excluding deletions, MRD-negative ETV6::RUNX1 patients with &#x2265;3 off-target RAG-mediated SVs had a >3-fold risk of relapse (hazard ratio:3.47, 95% CI:1.86-6.49). RAG-mediated SVs were also associated with relapse risk in T-cell ALL patients. Off-target RAG-mediated SV burden at diagnosis is a risk factor of relapse in pediatric ALL across molecular subtypes and independent of MRD status.

Journal Article↗
PubMed1978

Long-term antibody synthesis in vitro. VI. Anti-allotype sera as probes of clonal products in affinity maturation.

A new experimental system is described for measuring the allotypic product of rabbit B cells during long-lasting in vitro antibody responses. The immunoenzymatic assays described allow determination of several parameters mapping in different regions of the same molecule, which can be measured and combined to yield a multidimensional picture of the time-course dynamics of antibody synthesis. The rabbit immune system responding to Escherichia coli beta-D-galactosidase was sample and disassembled by (a) culturing lymph node microfragments and (b) sorting out from among all anti-enzyme antibodies only those activating a mutant enzyme, AMEF, which bore the b4 or b9 allotype. A considerable simplification of the response was achieved in the microcultures as documented by cultures of heterozygous cells which produced only one allotype and by the fact that each culture showed a distinctive pattern when antibody titre, association constant, heterogeneity index, L-chain type, and k-chain allotype were considered together. This array of patterns was not an artifact but the result of disassembling a representative sample of the rabbit immune system into small components, since the b4/b9 ratio obtained by averaging the results of all cultures from a heterozygous rabbit lymph node was the same as the serum ratio. Despite the Poisson distribution of the responder microcultures, none of them was monoclonal; i.e. no antibodies homogeneous by all parameters tested were observed, This finidng supports the notion that in normal lymphoid tissue in its native tridimensional arrangement, one T cell can trigger several B cells clustered in one antibody-forming unit. This natural arrangement would ensure the monospecificity of the cluster (dictated by the T cell) while allowing for variation in affinity (depending upon the array of B cells in the unit). Accordingly our findings would results from the fact that as the size of the microfragments was reduced, the cells diluted out first were T cells, but as long as one of them was present, several B-cell clones were triggered. The b4/b9 pattern of any given culture remained constant over several months, but the ratio kappa/lambda underwent changes. An increase in molecules with non kappa-chains (which could not be reacted with anti-kappa-chain allotype antisera) was usually associated with a parallel decrease in antibody affinity. This occurred by the end of the antibody cycle and might be related to the regulation of antibody synthesis by T-cell suppressor factors.

Animals↗
PubMedDate not supplied

[HBs-antigenemia and the state of cellular and humoral immunity in children with chronic viral hepatitis B].

In chronic virus hepatitis B the causative virus replicates for a long time as manifested by HBsAg persistence. Examinations of 92 sick children revealed changes in cellular and humoral immunity indices. The content of T-lymphocytes (determined according to Bach et al.) was reduced to 31.5 +/- 1.4% in the exacerbation stage (the normal content 50.8 +/- 1.3%), the percentage of O-cells increased, while the number of B-cells according to Mendes et al. did not change significantly. The inhibition of adhesion of A-cells (Halliday et al.--A. F. Blyuger) and "immune" plaque formation (according to A. F. Blyuger) in the presence of HBsAg were also increased maximally in the exacerbation stage. HBs-antigenemia was found to occur most frequently in the exacerbation stage. The content of immunoglobulin G was reduced. An increase in the number of tissue lymphocytes and their blast forms (in the "skin window" sample by Rebuck) was demonstrated. The authors assume that the long-term persistence of HBs-Ag and, consequently, the maintenance of the pathologic process activity are due to a defficiency of cellular immunity factors. The prospects of enhancing cellular immunity in virus hepatitis B in children are discussed.

Adolescent↗
PubMed1976

Analysis of immunosuppression generated by the graft-versus-host reaction. II. Characterization of the suppression cell and its mechanism of action.

Spleen cells from (CBA X C57/BL) F1 mice undergoing graft-versus-host (GVH) reaction induced by injection of parental cells 7-14 days previously are capable of suppressing an immune response by normal or primed F1 spleen cells to chicken erythrocytes and levan in vivo and sheep erythrocytes in vitro. The cells in these GVH spleens which were responsible for the suppression were sensitive to treatment with anti-0 serum, resistant to 900 rad irradiation in vivo and not retained by anti-immunoglobulin columns. Suppressor activity in vitro was present only in the non-adherent fraction of these GVH cell suspensions. Furthermore, the T-cell fraction, purified by affinity chromatography, suppressed the in vitro response of macrophage-depleted normal F1 cells to DNP-levan. Collectively, these observations imply that suppressor T cells generated by GVH reaction can affect B-cell functions directly without intermediary macrophage participation. Spleen cells from (CBA X C57/BL) F1 mice undergoing GVH reaction induced by C57/BL cells were depleted of their F1 content by treatment with anti-CBA alloantiserum. The suppressive activity of the residual donor component was still expressed against other F1 cells (AKR X C57/BL) which were H-2 compatible with the original host, but not against H-2-incompatible cells (DBA/1 X C57/BL) F1. However, the latter were suppressed in the presence of (CBA X C57/BL) F1 cells. Thus, interaction of donor T cells with F1 target cells containing those H-2 antigens towards which they are sensitized is mandatory for the subsequent manifestation of immunosuppressive activity. GVH cells suppressed the response of primed F1 cells in double Marbrook chambers when the two populations were separated were by a cell-impermeable membrane, provided the GVH suspension contained F1 cells to which donor T cells were sensitized. This suggests that soluble factors are involved in the mechanism of GVH-induced immunosuppression.

Animals↗
PubMed1975

[Diagnosis and therapy of primary defects of immunity (author's transl)].

Immunological responses are divided into those mediated by humoral antibody (B-Cells) and those by cells (T-Cells). Both depend upon the activity of small lymphocytes which become thymus or bursa analogue dependent during embryonic development. Primary immundeficiencies are therefor defects of lymphocytes attributed in most cases to gene defects. Early diagnosis is the necessary prerequisit for possible treatment. Tests for assessing the cellular immune status are: skin testes and in vitro tests. Clinical syndroms are: lymphocytopenia, hypoplasia, deficiency of lymphocytes in lymphatic tissues normal cortical germinal centres. Recurrent infections with viruses, candida or pneumocystis carinii are common. Tests for assesing the humoral immune status are: measurement of immunglobulin levels in serum, isohaemagglutinins, tests for antibody formation following active immunization, in vitro tests. Clinical syndroms are: no germinal centres in lymphnodes, no plasma cells. Recurrent bacterial infections. Treatment of B-cell deficiencies: immunglobulin replacement therapy. Treatment of T-cell deficiencies by grafting of thymus transplants. Combined immune deficiencies are treated with bone marrow transplants from matched donors. For bone marrow transplantation germfree state seems to be the ideal situation to protect the patient against infection before the therapeutic maneuver and for prevention of graft versus host reaction in the posttransplantation period.

B-Lymphocytes↗
PubMed1975

Analysis of immunosuppression generated by the graft-versus-host reaction. I. A suppressor T-cell component studied in vivo.

The kinetics and cellular characteristics of immunosuppression in (CBA-p X C57/Bl)F1 mice during graft-versus-host (GVH) reaction induced with spleen cells from either parental strain have been investigated. Effects on PFC responses to thymus-dependent (chicken red blood cells) and independent (levan) antigens have been compared. The unresponsive state which developed in GVH mice was expressed to comparable extent by their spleen cells following transfer to irradiated recipients. Furthermore, GVH spleen cells suppressed normal spleen cells in a mixed transfer system, but this effect was lost completely by day 21 whereas the original donors (or their cells) were still totally refractory after 80 days. This active suppressor effect was found to be mediated by T cells of perental origin based on cell fractionation analysis and selective deletion of donor or host cells by alloimmune attack. The delayed transfer of GVH cells to irradiated repopulated recipients challenged with antigen, indicated that suppressor T cells exert an anti-mitotic influence on antigen-stimulated B-cell proliferation. Supplementation of macrophage-depleted, anti-theta-treated GVH spleen cells with purified normal T cells demonstrated that B cells in GVH mice are normally reactive even when active suppression by T cells is no longer demonstrable. The likelihood that this later phase of immunosuppression is attributable to another mechanism is discussed.

Animals↗
PubMed1977

Immunological events at the surface of basophil granulocytes and mast cells which induce degranulation.

IgE molecules combine with basophil granulocytes and mast cells through the Fc portion and sensitize these cells for reaginic hypersensitivity reactions. The number of receptors for IgE per human basophil granulocyte is estimated to be 40,000 to 100,000 and those on rat mast cells is about 300,000. The binding of IgE with the receptor is reversible and does not involve covalent bonding. The affinity of IgE molecules for the receptors is high; the equilibrium constant of the reaction is in the order of 10(9)/mole for both human basophils and rat mast cell systems. Such a high affinity will explain why a minute amount of IgE antibody can sensitize the target cells and why sensitization with the antibody is so persistent. The initial step of the reaginic hypersensitivity reactions is probably bridging of cell-bound IgE molecules by antigen, which activates enzymatic sequences. The release of chemical mediators, however, is controlled by pharmacological factors which have most important rôles in transducing immunological signals into intracellular signals and subsequent biochemical processes.

Animals↗