ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1986.tb01936.x

出版商:Blackwell Publishing Ltd    

年代:1986

数据来源: WILEY

摘要:

The availability of paired homogeneous la+tumour cell lines (P388AD, interleukin (IL)‐l+and P388NA. IL‐1). which differ in inducibility for IL‐l, provided it unique opportunity to assess directly the role of Ia and IL.‐1 in the induction of cytolytic T cells (CTL) to trintrophenol (TNP)‐modified self. TNP‐P388AD but not TNP‐P388NA consistently induced Unrestricted, hapten‐specific CTL. However, in the presence of an exogenous source of IL‐l. TNP‐P388NA was able to induce CTL of the magnitude seen with TNP‐P388AD. Both Ia expression and IL‐l secretion were necessary in that when TNP‐modified purified T cells were utilized as stimulators, CTL activity was not demonstrated even if IL‐1 was added, but was only seen when unmodified. P388AD. or spleen cells

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1986.tb01937.x

出版商:Blackwell Publishing Ltd    

年代:1986

数据来源: WILEY

摘要:

We have recently described a heat‐labile and cell‐directed neutrophil migration inhibitory activity that is present in serum from patients with chronic lymphocytic leukaemia (CLL). The inhibitory activity is produced and secreted by CLL cells in vitro. In the present study the inhibitory activity was partially purified from short‐term cultures of monoclonal leukaemic B‐CLL cells. on gel filtration the calculated molecular weight was apparently 30,000. By anion exchange chromatography, the inhibitory factor was recovered in the fractions that eluted with 0.3 mol/l NaCl. The active material applied to preparative agarose gel electrophoresis migrated towards the anode. The inhibitory factor was totally destroyed by trypsin. In addition it bound to concanavalin A‐Sepharose. These properties indicate that the inhibitory factor is a glycoprotein. Antibodies against the isolated inhibitory factor were raised in rabbits. CLL serum was separated by means of gel filtration and the inhibitory activity was recovered in the pool with a molecular weight of approximately 30,000. The activity was completely neutralized by the antibodies raised against the CLL‐cell‐derived inhibitor, indicating the similarity between this and the serum‐derived inhibitor. We have shown the existence of a new lymphokine, derived from B‐CLL cells, in serum from

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1986.tb01938.x

出版商:Blackwell Publishing Ltd    

年代:1986

数据来源: WILEY

摘要:

Human monocyte‐depleted peripheral blood mononuclear cells were separated in T4+and T8+populations by a panning technique. Petri dishes coated with goat anti‐mouse antibodies were plated by peripheral blood mononuclear cells coated by monoclonal antibodies, either T4 or T8. The cell populations were separated into adherent and non‐adherent populations based on binding to the goat anti‐mouse‐coated plastic dishes. The purity of the adherent populations was 96%. T4+and T8+populations were used as effector cells in the concanavalin A‐induced suppressor test. The T4+population revealed a pronounced suppressor activity similar to that exhibited by the T8+population. This finding was independent of two different sources of monoclonal antibodies, T4/T8 and OKT4/OKT8. The registered suppressor activity in the monoclonal antibody‐defined helper population could not be explained either by a switch of the membrane phenotype from T4+to T8+cells or by an increased interleukin 2 consumption of the concanavalin A

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1986.tb01939.x

出版商:Blackwell Publishing Ltd    

年代:1986

数据来源: WILEY

摘要:

Immature monocytes residing m the spleens of newborn nine less than 6–7 days of age are known to suppress T‐dependent; and T‐independent immune responses in vitro and in vivo. Suppression is mediated in part through products secreted In the newborn monocytes, In the present study. we have identified 3 monokines secreted by newborn, but not adult, monocytes correlating with materials possessing significant suppressor activity in vitro. These monokines have molecular weights of 5N. 58. 10.8. and 10 kilodaltons. appear to be proteins, and are insensitive to heat inactivation. The 58 kd material is antigenically distinct from alpha‐fetoprotein. while the lower molecular weight materials arc too large to be prostaglandins. Although these monokines can he shown to have activity in vitro, they are not as efficient as newborn monocytes in preventing alloreactivity

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1986.tb01940.x

出版商:Blackwell Publishing Ltd    

年代:1986

数据来源: WILEY

摘要:

The rapid loss of alloreactivity within populations of antigen‐primed, in vitro propagated T cells cannot he explained by the appearance of suppressor cells nor by the dilution effect of the proliferative antigen‐specific T cells alone. The involvement of trans‐stimulation in loss of alloreactivity, i.e. the recruitment of non‐antigen‐specific T cells into proliferation in an antigen‐dependent and specific fashion, was assessed. Susceptibility to trans‐stimulation was found to correlate directly with stale of activation at the outset of assay. Large T cells (low buoyant density) hut not small T cells (high buoyant density) are susceptible lo trans‐stimulation. Moreover, in vitro pre‐activation of small T cells by mitogen confers susceptibility to trans‐stimulation. Analysis of lire alloreactivity in Percoll fractions of antigen‐primed lymph node T cells revealed activity in both large‐ and small‐T‐cell fractions with some enrichment in the latter. The small T cells, refractive to trans‐stimulation, are diluted out of the population within the early weeks of antigen‐mediated in vitro propagation, accounting for a rapid loss of considerable alloreactivity. The loss of all delectable alloreactivity within antigen‐selected populations suggests that the slate of activation conferring sensitivity to trans‐stimulation must be maintained, and that neither the antigen nor the culture condi

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1986.tb01941.x

出版商:Blackwell Publishing Ltd    

年代:1986

数据来源: WILEY

摘要:

We have previously reported a case ot Sezary Syndrome (SS), in which an OKT4‐ T‐cell population exhibited a defective response to non‐specific mitogens, and an ability In suppress lectin‐induced T‐cell proliferation and pokeweed mitogen (PWM)‐induced B‐cell differentiation of normal donor peripheral blood mononuclear cells (PBMC) We report now that resting Sézary cells (SC) were essentially negative for activation activation (Ag) detected by monoclonal antibodies (MoAb) BI. 49.9. anti‐Tac. OKT9.OKT10. and OKIal. After phytohaemagglutin (PHA) stimulation, all these Ag were expressed With the notable exception of OKT10. Further investigations of SC functions indicated that no inlerleukin2(IL.‐2) biological activity was detected in culture supernalanls ot SC costimulated with PHA and phorbol myristate acetate (PMA). Interestingly, such stimulated SC exhibited a marked capacity to absorb exogenous IL‐2 while remaining unable to proliferate. These data suggest that patient's unresponsiveness to PHA may be unrelated to IL‐2 as an extracellular growth signal, but may instead be due to a failure in a later cellular activation event, subsequent to the binding of IL‐2 to its receptors. Lack of T10 Ag expression may be involved as a cause or a consequence. Kinetic study of suppression of PHA‐induced T‐cell proliferation of normal PBMC revealed that inhibition occurred during the first 24 h; moreover we showed that it was not due to limitation of available IL‐2 since it persisted in excess of IL‐2: remarkably the growth of an IL.‐2‐dependent murine cell line was unaffected by the presence of SC Further, inhibition was also observed on IL.‐2 independent calcium ionophore A 23187‐indueed T ‐cell proliferation of normal PBMC Taken together, the data suggest that the target of suppressor activity is probably an important ohligarory intracellular event controlling DNA replication, which is common to both IL.‐2‐Independent and IL‐2‐dependent T‐cell activation processes Human T‐cell leukaemia/lymphoma virus I (HTLV‐1) related p.19 and p.24 Ag were absent on fresh and.10‐day cultured SC. suggesting the absence of HTI.V‐1 infection,

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1986.tb01942.x

出版商:Blackwell Publishing Ltd    

年代:1986

数据来源: WILEY

摘要:

The binding of complement (C)‐solubilized125I bovine serum albumin (BSA) anti‐BSA immune complexes (IC) to CR1 receptors on human red blond cells (RBC‐CR1) was studied. The binding of IC to CRI was strongly dependent on the molar antigen lo antibody ratio, and IC formed in moderate antigen excess showed no binding. IC solubilized, in 50% human serum in the presence of autologous RBC bound rapidly lo RBC‐CRI, with maximal binding within less than 1 min at 37°C. Release of CRI‐hound IC under these conditions occurred slowly, requiring more than.30 min. Only binding of ‘partially’ solubilized, e.g., anti C3c (C4c) and conglutinin‐reactive 1C occurred, whereas fully solubilized complexes (IC‐C3dg. C4d) showed virtually no binding. Solubilization of IC in the presence of Mg‐EGTA or in C2‐deficient serum resulted in a markedly delayed binding of IC ti RBC, indicating the importance of an intact classical pathway in preparing the IC for binding to RBC‐CR1. C‐solobilized IC could be absorbed to solid‐phase conglutinin or antibody to C3c abd C4c, and tgese kugabds were able to inhibit the binding of solubilized IC to RBC. Heparin also exerted a marked, dose‐dependent inhibitory effect on the binding of presolubilized IC to RBC‐CR1, whereas the binding was unaffected by the addition of monosaccharides or by the

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1986.tb01943.x

出版商:Blackwell Publishing Ltd    

年代:1986

数据来源: WILEY

摘要:

Lymphocytes from rats sensitized with basic protein (BP) plus complete Freund's adjuvant (CFA), which produce allergic encephalomyelitis when transferred to adult recipients, fail to induce disease when transferred to 3‐ to 5‐day‐old neonatal rats. The transferred cells do, however persist in the recipients and can be revealed by actively challenging with BP‐CFA later in adult life. Challenge leads to a significantly earlier onset of disease than is seen in control animals. We report here that the cells are long lived and persist in the recipients for at least 9 months. The cells can be demonstrated in the spleen and lymph nodes of recipient animals and can be activated by homologous and cross‐reacting encephalitogenic antigenic preparations but not by antigen in nonencephalitogenic forms. These neonatal recipients, which carry autoimmune effector cells asymptomatically for prolonged periods, may provide a useful model for advancing our understanding of immunoregulatory events in this experimental demyelinating disease as well as the human demyelinating disease multiple

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1986.tb01944.x

出版商:Blackwell Publishing Ltd    

年代:1986

数据来源: WILEY

摘要:

Cellular changes in the liver were studied during an acute lethal graft‐versus‐host (GVH) disease in relation to the expression of major histocompatibility complex (MHC) antigens on different liver cells‐ Screening for MHC antigen expression revealed that control livers contained very few Ia+ cells: mainly cells in the portal tract interstitium and and a small percentage of the Kupffer cells. The changes during an ongoing GVH reaction could he separated into those related to the sinusoid‐associated cells, including the liver parenchyma, and those related to the portal‐tract‐associated cells, including periportal hepalocytes In the sinusoids an increase in the number of Kupffer cells was seen, mm all expressing Ia+antigens No damage to hepatocytes or other sinusoid‐associated cells was observed 1l is postulated that the increase in both number and Ia+expression of the Kupffer cells is most probably due to an increased phagocytic uptake of Mood‐borne cellular debris and is not a result of extensive damage to hepatocytes. In the portal tracts expanding infiltrates were found composed of Ia+T ceils and macrophages (ratio 2:1). These infiltrates are probably due to a local accumulation of lymphocytes and macrophages as a result of an interaction of migrating donor‐type alloreactive T cells with recipient type Ia+cells present in the portal tract interstitium. which also interfered with normal recipient lymphocyte and macrophage traffic. Damage to portal‐tract‐associated cells was slight and confined to bile duct epithelial cells, which now expressed Ia+antigens, and to periportal hepatocytes. In conclusion, these data do not indicate that damage to liver parenchyma plays a major role in the pathogenesis of

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1986.tb01945.x

出版商:Blackwell Publishing Ltd    

年代:1986

数据来源: WILEY