Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “MACROPHAGES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed1995

Macrophage colony-stimulating factor induces thrombospondin 1 production by cultured human macrophages.

The role of colony-stimulating factors (CSFs) in regulating the synthesis of thrombospondin 1 (TSP1) by cultured human macrophages is investigated. Macrophage (M)-CSF is shown rapidly and transiently to induce two predominant species of TSP1 mRNA. One of these species was 3.2 kb in size and appeared to be specific to M-CSF-stimulated macrophages. Adherent M-CSF-treated macrophages are also shown to express abundant surface cell-associated TSP rapidly when examined by indirect immunofluorescence staining. Granulocyte-macrophage (GM)-CSF induced TSP1 mRNA at a later time point, and this was attributable to the effects of endogenous M-CSF induced by the GM-CSF; the GM-CSF-treated cells did not display surface-associated TSP after 3 hr of treatment. Analysis of the TSP1 protein synthesised by the M-CSF-treated macrophages revealed the expected trimeric form of the molecule. In addition, an unidentified 95-kDa protein was found to be covalently associated with immunoreactive TSP1, and this appeared to be specific to the macrophages as it was not found in TSP1 precipitated from other cell types. It is suggested that the induction of TSP1 by M-CSF may play an important role in the major physiological functions of macrophages.

Cells, Cultured↗
PubMed1984

Functional characteristics of the macrophage receptors for IgG-Fc and C3: failure to detect C3 receptor-mediated extracellular cytolysis by mouse peritoneal macrophages.

The ability of several immunologic ligands to mediate extracellular cytolysis of sheep erythrocytes (E) by mouse macrophages was studied. E coated with rabbit IgG (EIgG), but not nonsensitized E or E coated with rabbit IgM (EIgM), were lysed and phagocytized by resident peritoneal macrophages as well as by macrophages activated in vivo with either BCG or Corynebacterium parvum or in vitro with lymphokine. EIgM incubated with mouse serum to deposit the third component of complement (C3) onto E (EIgMC) were ingested by thioglycolate-elicited and lymphokine-treated macrophages, but not by the other macrophage populations examined. However, none of the macrophages performed lysis of EIgMC, suggesting that engagement of macrophage C3 receptors by target cell-bound C3 was not a sufficient trigger for cytolysis. Lysis of E coated with both IgG and C3 (EIgGC) was moderately elevated over that of EIgG; this enhancement was not abolished after proteolytic destruction of the macrophage C3-rosetting capacity, indicating that C3 receptors were not responsible. EIgGC and EIgMC were more susceptible to hypotonic lysis than were either E, EIgG, or EIgM, suggesting that enhanced lysis of serum-treated E may be partially explained by increased E fragility.

Animals↗
PubMed1995

Effect of vitamin E succinate on smokeless tobacco-induced production of nitric oxide by rat peritoneal macrophages and J774A.1 macrophage cells in culture.

Previous studies have shown that an aqueous smokeless tobacco extract when administered in a single oral dose to rats results in an enhanced induction of hepatic lipid peroxidation, hepatic DNA single strand breaks, and a marked increase in the urinary excretion of the lipid metabolites malondialdehyde, formaldehyde, acetaldehyde, and acetone. These observations strongly suggest that STE induces the production of reactive oxygen species. We have therefore examined the effects of STE in vivo in rats on the production of nitric oxide (NO) by isolated peritoneal exudate (macrophage) cells and when incubated with cultured J774A.1 macrophage cells. In both cases, a significant increase in NO production was observed. When the antioxidant vitamin E succinate was preadministered to rats, a marked decrease in NO production in response to STE by isolated peritoneal macrophages was observed. Similar results were observed when J774A.1 macrophages were cultured in the presence of vitamin E succinate and STE. When vitamin E succinate alone was cultured with macrophages, an increase in NO production was observed. A similar increase was observed when the vitamin E succinate was administered to rats, and NO production by isolated peritoneal macrophages was assessed. The results demonstrated that the increase in NO production by macrophages in response to vitamin E succinate was due to a succinate moiety. Taken together with previous studies, the results indicate that STE activates macrophages, which result in the production of reactive oxygen species. These reactive oxygen species may be responsible for tissue damaging effects including lipid peroxidation and DNA damage, which may be associated with the cytotoxicity and mutagenicity of smokeless tobacco products.

Animals↗
PubMed1997

Intravenously administered macrophage colony-stimulating factor (M-CSF) specifically acts on the spleen, resulting in the increasing and activating spleen macrophages for cytokine production in mice.

IL-6 was transiently expressed in sera of mice after a bolus intravenous injection with LPS and it peaked 2 h later. Intravenous administration of M-CSF at 250 micrograms/kg/day for 5 days prior to an injection of 25 micrograms/kg of LPS elevated the serum IL-6 level 10-fold higher than that of mice which were not given M-CSF. Although M-CSF had no effect on the number of macrophages in alveoli and peritoneal cavity, it tripled the number of spleen macrophages and increased macrophage-progenitor cells 7-fold when injected intravenously. Spleen macrophages from M-CSF-injected mice produced 5-fold more IL-6 in response to LPS-stimulation in-vitro. However, M-CSF-injection had lesser effects on LPS-induced IL-6 production from liver, alveolar and peritoneal macrophages. Exogenously administered M-CSF was detected at higher concentration and for longer duration in the spleen than in any other organs examined. Spleen macrophages incubated in-vitro with more than 1000 U/ml of M-CSF for 3 days also produced more LPS-induced IL-6 than untreated cells. These results indicate that intravenously administered M-CSF not only enhances macrophage development in the spleen, but also primes mature macrophages for cytokine production.

Animals↗
PubMed2003

Blockade of macrophage colony-stimulating factor reduces macrophage proliferation and accumulation in renal allograft rejection.

Macrophage accumulation within an acutely rejecting allograft occurs by recruitment and local proliferation. To determine the importance of M-CSF in driving macrophage proliferation during acute rejection, we blocked the M-CSF receptor, c-fms, in a mouse model of acute renal allograft rejection. C57BL/6 mouse kidneys (allografts, n = 20) or BALB/c kidneys (isografts, n = 5) were transplanted into BALB/c mice. Anti-c-fms antibody (AFS98) or control Ig (50 mg/kg/day, i.p.) was given daily to allografts from days 0-5. All mice were killed day 6 postoperatively. Expression of the M-CSF receptor, c-fms, was restricted to infiltrating CD68+ macrophages. Blockade of c-fms reduced proliferating (CD68+/BrdU+) macrophages by 82% (1.1 v 6.2%, p < 0.001), interstitial CD68+ macrophage accumulation by 53% (595 v 1270/mm2, p < 0.001), and glomerular CD68+ macrophage accumulation by 71% (0.73 V 2.48 CD68+ cells per glomerulus, p < 0.001). Parameters of T-cell involvement (intragraft CD4+, CD8+ and CD25+ lymphocyte numbers) were not affected. The severity of tubulointerstitial rejection was reduced in the treatment group as shown by decreased tubulitis and tubular cell proliferation. Macrophage proliferation during acute allograft rejection is dependent on the interaction of M-CSF with its receptor c-fms. This pathway plays a significant and specific role in the accumulation of macrophages within a rejecting renal allograft.

Animals↗
PubMed1987

Human macrophage-activating factors for cytotoxicity. I. Establishment of a human T-cell hybridoma that produces macrophage-activating factors for cytotoxicity.

Human T cell hybridoma, H3-E9-6, that produces macrophage activating factors for cytotoxicity (MAF-C) was prepared by somatic fusion of phytohemagglutinin-activated peripheral blood lymphocytes with emetine/actinomycin D-treated cloned human acute lymphocytic leukemia cells (CEM 11). The activities of the following were assayed: (1) macrophage-activating factor for cytotoxicity of monocytes (MAF-C 1 day), (2) macrophage-activating factor for cytotoxicity of monocyte-derived macrophages (MAF-C 6 day), (3) macrophage-activating factor for cytotoxicity of murine macrophages (MAF-Cm), (4) macrophage-activating factor for glucose consumption (MAF-G), (5) macrophage-activating factor for O2- formation (MAF-O). The culture supernatant of H3-E9-6 showed MAF-C 1 day-MAF-C 6 day, MAF-Cm, and MAF-G activities. The MAF-Cm activity was considerably enhanced by the addition of murine recombinant interferon gamma (rIFN-gamma). The MAF-C 1 day activity in the H3-E9-6 sup was not decreased by heat treatment (56 C, 30 min), by pH 2 treatment or by the addition of monoclonal anti-human IFN-gamma antibody or polymyxin B. These data suggest that MAF-C in H3-E9-6 sup is distinct from human IFN-gamma or lipopolysaccharide (LPS).

Cytotoxicity, Immunologic↗
PubMed1995

Relationship between granulocyte macrophage-colony stimulating factor, tumour necrosis factor-alpha and Trypanosoma cruzi infection of murine macrophages.

Gamma interferon (IFN-gamma)-activated macrophages control Trypanosoma cruzi infection via nitric oxide (NO), recently recognized as a major effector molecule. Granulocyte macrophage-colony stimulating factor (GM-CSF) is a multipotent cytokine secreted by macrophages and many other cells. It induces the production of tumour necrosis factor alpha (TNF-alpha), another cytokine also secreted by macrophages and involved in the control of T. cruzi infection. However, no data are available on the relationship between GM-CSF, TNF-alpha and NO produced by macrophages activated by IFN-gamma and infected with T. cruzi. To highlight this relationship, mouse peritoneal macrophages (MPM) and two c-myc retrovirus-induced macrophage cell lines (9.1.1 and BMM8), respectively characterized by a constitutive and an inducible production of GM-CSF, were activated with IFN-gamma and/or GM-CSF and infected with T. cruzi. Our results indicate that T. cruzi upregulates GM-CSF release from MPM and from the two macrophage cell lines, activated (or not) by IFN-gamma. A high autocrine production of GM-CSF or an exogenous supply of GM-CSF is correlated with an enhanced release of TNF-alpha and NO, inducing an improved control of T. cruzi infection by IFN-gamma-activated MPM.

Animals↗
PubMed2003

PU.1 regulation of human alveolar macrophage differentiation requires granulocyte-macrophage colony-stimulating factor.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is critically implicated in lung homeostasis in the GM-CSF knockout mouse model. These animals develop an isolated lung lesion reminiscent of pulmonary alveolar proteinosis (PAP) seen in humans. The development of the adult form of human alveolar proteinosis is not due to the absence of a GM-CSF gene or receptor defect but to the development of an anti-GM-CSF autoimmunity. The role of GM-CSF in the development of PAP is unknown. Studies in the GM-CSF knockout mouse have shown that lack of PU.1 protein expression in alveolar macrophages is correlated with decreased maturation, differentiation, and surfactant catabolism. This study investigates PU.1 expression in vitro and in vivo in human PAP alveolar macrophages as well as the regulation of PU.1 by GM-CSF. We show for the first time that PU.1 mRNA expression in PAP bronchoalveolar lavage cells is deficient compared with healthy controls. PU.1-dependent terminal differentiation markers CD32 (FCgammaII), mannose receptor, and macrophage colony-stimulating factor receptor (M-CSFR) are decreased in PAP alveolar macrophages. In vitro studies demonstrate that exogenous GMCSF treatment upregulated PU.1 and M-CSFR gene expression in PAP alveolar macrophages. Finally, in vivo studies showed that PAP patients treated with GM-CSF therapy have higher levels of PU.1 and M-CSFR expression in alveolar macrophages compared with healthy control and PAP patients before GM-CSF therapy. These observations suggest that PU.1 is critical in the terminal differentiation of human alveolar macrophages.

Bronchoalveolar Lavage Fluid↗
PubMed1985

Different mechanisms of macrophage activation with guinea pig macrophage activation factor, lipopolysaccharide and muramyl dipeptide.

The mechanism of macrophage activation was studied using three activating substances, guinea pig macrophage activation factor (MAF), lipopolysaccharide (LPS) and muramyl dipeptide (MDP). Guinea pig peritoneal exudate macrophages were activated to exhibit the accelerated glucose consumption in response to these activating substances. Calmodulin-specific inhibitors, trifluoperazine and No. 233, inhibited macrophage activation with MAF and LPS, while these inhibitors did not affect the activation with MDP. Ca2+ uptake into macrophages was enhanced in MAF-treated macrophages, but LPS and MDP did not affect the Ca2+ uptake. Methylamine and ethylamine, inhibitors of transglutaminase-dependent protein internalization into cells and/or of lysosomal enzymes, effectively inhibited the activating effect of LPS, but not those of MAF and MDP. These results suggest that Ca2+ and calmodulin play a role in macrophage activation with MAF, and neither transglutaminase-dependent internalization nor lysosomal enzymes participate in the activation process. In case of LPS, internalization into cells would be necessary for its activating effect. The processing of the contrary, since the activating effect of MDP was not affected by any of these inhibitors, the mechanism of activation with MDP remains obscure. Thus, the mechanisms of macrophage activation with MAF, LPS and MDP appear to be different from each other.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed2002

The role of ceramide of human macrophage gangliosides in activation of human macrophages.

Gangliosides of macrophages have immunoregulatory and structural attributes, distinct from neural gangliosides. We previously produced a monoclonal antibody to human macrophage gangliosides (HMG; mAb25F4), which inhibited macrophage migration and recognized a surface-accessible epitope. We investigated expanded immunoregulatory properties and molecular domains for antibody recognition. mAb25F4 directly induced human macrophage production of proinflammatory cytokines, interleukin-1beta, and tumor necrosis factor alpha. Conditions were established for selective, reversible depletion of HMG with D-threo-(R,R)-1-phenyl-2-decanoyl-amino-3-morpholine-1-propanol. mAb25F4 had diminished recognition for ganglioside-depleted macrophages, which was restored with regeneration of gangliosides. Although desialylation of HMG did not impair mAb25F4 recognition, enzymatic cleavage of ceramide abolished antibody binding. Antibody recognition was specific for the ceramide fraction, with preferential recognition for ceramide of HMG and murine macrophage gangliosides and limited recognition for neural tissue ceramide and gangliosides. This study underscores the importance of structurally distinct ceramide of macrophage gangliosides as a critical domain for ganglioside-mediated activation of human macrophages.

Animals↗
PubMed1990

Enhanced stimulation of human bone marrow macrophage colony formation in vitro by recombinant human macrophage colony-stimulating factor in agarose medium and at low oxygen tension.

Recombinant (r) and natural human (h) macrophage colony-stimulating factor (M-CSF, CSF-1) have been considered poor stimulators of macrophage progenitor cells present in human marrow, although they are potent stimulators of these cells in mouse marrow. We compared the growth characteristics of rhM-CSF-responsive human macrophage progenitor cells placed in semisolid agarose or agar culture medium and incubated for 14 days at ambient (approximately 20%) or lowered (5%) O2 tension. By itself, rhM-CSF was found to be a good stimulator of macrophage colony formation by human bone marrow cells cultured in agarose but not in agar; this growth was enhanced by incubation at 5% O2. Maximal numbers (up to 115/10(5) nonadherent low density cells plated) of macrophage colonies (50 to greater than 500 cells per colony) were stimulated by 500 to 1,000 units rhM-CSF/mL, with 1/2 maximal numbers stimulated by 250 to 500 units/mL. With agarose as the support medium, rhM-CSF was two- to fourfold more active on mouse than on human macrophage colony formation, in contrast to previous reports of 10- to 100-fold greater activity when agar was used as the support medium. Using nonadherent low density T lymphocyte-depleted human bone marrow cells growing in agarose at 5% O2, greater than additive effects on colony formation were observed when 31 to 500 units rhM-CSF were used in combination with either 10 ng rh interleukin-1 alpha (IL-1 alpha), 20, or 200 units rh granulocyte-macrophage (GM)-CSF or rhG-CSF. The agarose assay system should be useful for evaluating factors regulating the proliferation of human macrophage progenitor cells in vitro and during clinical trials with rhM-CSF.

Agar↗
PubMed1991

Granulocyte-macrophage colony-stimulating factor is a major macrophage fusion factor present in conditioned medium of concanavalin A-stimulated spleen cell cultures.

In 1983, we reported that the conditioned medium (CM) of spleen cell cultures treated with Con A greatly induced fusion of mouse alveolar macrophages within 2 to 3 days at a very high rate of more than 80% (Proc. Natl. Acad. Sci. USA 80:5583, 1983). In the course of examining macrophage fusion factors (MFF) present in Con A-CM, we found that IL-4 induced fusion of alveolar macrophages with a time course similar to that induced by Con A-CM. However, the maximal fusion rate induced by IL-4 (4 ng/ml) was about 35%. Furthermore, the fusion induced by Con A-CM was blocked only partially by adding IL-4 antibody, indicating that there are unknown MFF other than in Con A-CM. Of several other cytokines produced by Con A-stimulated spleen cells, IL-6 (20 ng/ml), IFN-gamma (45 ng/ml) and granulocyte-macrophage (GM)-CSF (10 ng/ml) greatly potentiated the fusion induced by 4 ng/ml of IL-4. The assay of these cytokines in Con A-CM proved that it contained 0.44 +/- 0.04 ng/ml of IL-4, 1.0 +/- 0.24 ng/ml of IL-6, 9.1 +/- 0.07 ng/ml of IFN-gamma, and 11.6 +/- 1.66 ng/ml of GM-CSF. When the potentiating effects of IL-6, IFN-gamma and GM-CSF on macrophage fusion were examined in the presence of 0.4 ng/ml of IL-4, only GM-CSF increased the fusion rate to the maximal level induced by Con A-CM at its physiologic concentration (10 ng/ml). The macrophage fusion induced by Con A-CM was greatly suppressed by adding antibody against GM-CSF. GM-CSF had a biphasic effect on growth and fusion, depending on its dose levels used: 0.01 to 0.1 ng/ml increased proliferation without inducing fusion and 10 ng/ml preferentially induced fusion. There was a negative relationship between macrophage growth and fusion. IL-4 was a potent inhibitor of proliferation of macrophages induced by GM-CSF. These results clearly indicate that GM-CSF is a major MFF present in Con A-CM.

Animals↗
PubMed1990

Expansion of immunoregulatory macrophages by granulocyte-macrophage colony-stimulating factor derived from a murine mammary tumor.

Using an immunogenic nonmetastatic murine mammary adenocarcinoma (D1-DMBA-3) induced in BALB/c mice by dimethylbenzanthracene, we have previously shown that splenocytes from tumor bearers have depressed lymphocyte responses to mitogens and antigens, including tumor-associated antigens. In addition, they display decreased natural killer and T-cell cytotoxic activities. Macrophages from tumor-bearing mice appear to be responsible for the suppression of T- and B-cell responses to concanavalin A, lipopolysaccharide, and tumor-associated antigens observed in tumor bearers. The appearance of these macrophages in the spleen tightly parallels the progressive growth of the tumor and the concomitant immunosuppression. Simultaneously high levels of macrophage progenitors were observed in blood, bone marrow, lung, and liver. A significant increase of colony-stimulating activity of the granulocyte-macrophage lineage was detected in the sera from tumor-bearing mice. Higher levels of this colony-stimulating activity (CSA) were detected in tumor cystic fluid as compared with the levels in serum. A tumor cell line established in vitro from the D1-DMBA-3 in vivo tumor produces high levels of a factor with CSA in culture supernatant fluids. Partial purification of the CSA from the tumor cell line supernatants was achieved using CentriCell ultrafiltration and SephacrylS-300 chromatography. These studies revealed that the molecular weight of the colony-stimulating-like factor is 32,000 to 35,000. The morphology of the colonies obtained in cultures using this factor is similar to that of the colonies that develop in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) but not with macrophage colony-stimulating factor (M-CSF). CSA from tumor cell supernatants was neutralized by antiserum to GM-CSF but not with anti-M-CSF or anti-granulocyte colony-stimulating factor (G-CSF). Macrophages from bone marrow or peritoneal exudates from normal mice cultured with tumor supernatant for 2 to 3 days strongly inhibit normal splenocyte responses to concanavalin A and lipopolysaccharide. The data suggest that the tumor releases a GM-CSF that alters the hemopoietic system and induces or expands macrophages, which exert a suppressive function on the immune system of tumor-bearing mice.

Animals↗
PubMed1984

Macrophage activation to kill Leishmania tropica: defective intracellular killing of amastigotes by macrophages elicited with sterile inflammatory agents.

Resident peritoneal macrophages and macrophages elicited by injection of C3H/HeN mice with sterile inflammatory agents were exposed to amastigotes of Leishmania tropica in vitro and treated with lymphokines. Resident macrophages developed the capacity to kill intracellular parasites; microbicidal activity of activated resident cells ranged between 60 and 80%. In contrast, inflammatory macrophages responded poorly to lymphokines for intracellular killing of amastigotes; microbicidal activity of cells elicited with chronic inflammatory agents ranged between 0 and 45%. Defective intracellular killing of L. tropica by inflammatory macrophages was independent of the agent used to elicit the cells, but was clearly associated with the number of immature macrophages in the population. That intracellular killing capacity may reflect the presence of a killing mechanism in tissue-derived cells that is not yet developed in undifferentiated macrophages is supported by studies with peripheral blood monocytes: these cells were also incapable of eliminating intracellular amastigotes in the presence of potent activating factors. These observations on inflammatory macrophage interactions with amastigotes may provide important insights into the chronic nature of leishmanial disease.

Animals↗
PubMed1998

Macrophages kill T9 glioma tumor cells bearing the membrane isoform of macrophage colony stimulating factor through a phagocytosis-dependent pathway.

Rat T9 glioma cells transfected with the gene for the membrane isoform of macrophage-CSF (mM-CSF) but not for the secreted isoform of M-CSF were directly killed by bone marrow-derived macrophages. Macrophage-mediated cytolysis of the mM-CSF-transfected clone was blocked by using chemical inhibitors of phagocytosis such as iodoacetate, 2-deoxyglucose, gadolinium chloride, and cytochalasin B. In contrast, macrophage-mediated killing of mM-CSF-expressing tumor cells was augmented by the microtubule inhibitor, colchicine. Use of nitric oxide and reactive oxygen intermediate inhibitors failed to alter the macrophage-mediated killing of the mM-CSF-transfected tumor cells. Photomicroscopy, using immunohistochemical staining with the anti-Hck Ab to distinguish macrophages from tumor cells, revealed that phagocytosis began within 2 h after addition of the mM-CSF-bearing tumor cells. Photocinematography confirmed that macrophages first phagocytosized and then lysed the internalized mM-CSF transfectant cells. Using annexin V and acridine orange staining techniques, macrophages phagocytosized living mM-CSF-transfected tumor cells.

Animals↗
PubMed1998

Alternative macrophage activation-associated CC-chemokine-1, a novel structural homologue of macrophage inflammatory protein-1 alpha with a Th2-associated expression pattern.

We have cloned a novel human CC-chemokine, alternative macrophage activation-associated CC-chemokine (AMAC)-1. The isolated cDNA clone (803 bp) shows a single open reading frame of 267-bp coding for 89 amino acid residues; mature AMAC-1 protein is predicted to consist of 69 amino acids with a m.w. of 7855. Sequence alignment and 3D-modeling show the typical structural characteristics of CC-chemokines with special features in the receptor-activating domain. AMAC-1 is most closely related to MIP-1 alpha with a cDNA and protein sequence homology of 55% and 59%, respectively. However, the expression pattern of AMAC-1 is directly opposite to that of MIP-1 alpha. While MIP-1 alpha is induced by classical macrophage mediators such as LPS and is inhibited by IL-4 and glucocorticoids, AMAC-1 is specifically induced in macrophages by alternative macrophage mediators such as IL-4, IL-13, and IL-10. Expression of AMAC-1 is inhibited by IFN-gamma while glucocorticoids exert a slightly positive synergistic effect in combination with IL-4. Peripheral blood monocytes do not express AMAC-1; time course experiments show that monocyte-to-macrophage differentiation is a prerequisite for AMAC-1 expression. Expression of AMAC-1 by granulocyte-macrophage CSF/IL-4-induced, monocyte-derived dendritic cells is complex; in mature adherent dendritic cells, however, only minor AMAC-1 mRNA expression was found. In vivo, AMAC-1 is expressed by alveolar macrophages from healthy persons, smokers, and asthmatic patients. In conclusion, AMAC-1 is a novel CC-chemokine whose expression is induced in alternatively activated macrophages by Th2-associated cytokines; thus, AMAC-1 may be involved in the APC-dependent T cell development in inflammatory and immune reactions.

Amino Acid Sequence↗