ISSN:0004-945X    

DOI:10.1111/j.1440-1711.1991.tb03728.x

出版商:Blackwell Publishing Ltd    

年代:2017

数据来源: WILEY

摘要:

SummaryMice deficient in the fifth component of complement are known to be extremely susceptible to lethal challenge withCandida albicans.However, male mice, that have significantly higher concentrations of serum C5 than females, were markedly more susceptible to infection. This difference was observed in both susceptible (CBA/H) and resistant (BALB/c) mice. Levels of serum C3 likewise showed no correlation with susceptibility.

ISSN:0004-945X    

DOI:10.1038/icb.1991.2

出版商:Blackwell Publishing Ltd    

年代:2017

数据来源: WILEY

摘要:

SummaryPrevious reports have documented that mice bearing plasmacytomas (PC) are suppressed in their ability to mount a primary antibody response, whereas cellular immunity appears to be normal. Studies presented here provide evidence that T cell responsiveness is also depressed in BALB/c mice bearing the Lieberman plasmacytoma (Lpc‐1). For instance, splenocytes from mice bearing large tumours were impaired in theirin vitroability to respond to the T cell mitogen, mount an appropriate alloreactive cytolytic T lymphocyte response, and produce interleukin‐2 (IL‐2). A population of suppressor cells was detected in the spleens 7 days after tumour implantation as evidenced by their ability to prevent normal splenocytes not only from responding to antigens in mixed lymphocyte culture, but also from producing IL‐2. A similar inhibitory effect was observed with culture supernatants of these cells, indicating the existence of a soluble suppressive factor. Therefore, the present study demonstrates that cellular immune responses are impaired in mice bearing Lpc‐1 tumours and that this effect may be due to the generation of suppressor cells and/or a suppressive factor.

ISSN:0004-945X    

DOI:10.1038/icb.1991.3

出版商:Blackwell Publishing Ltd    

年代:2017

数据来源: WILEY

摘要:

SummaryThe effects were investigated of two pretreatments of human serum and plasma test samples on their subsequent reactivity in the anticardiolipin antibody enzyme‐linked immunosorbent assay (ACA‐ELISA).The first treatment involved heat inactivation of test samples at 56°C for 30 min, a process sometimes used to inactivate samples from suspected human immunodeficiency virus positive individuals. Such treatment significantly increased the IgG ACA unit/mL values of normal sera, but when this effect was examined further, it was found that the increase in binding occurred on both cardiolipin‐coated and uncoated wells and was therefore non‐specific. Heat inactivation of sera prior to ACA testing should therefore be avoided.The second treatment involved diluting immunoglobulin (ig)G and IgM ACA‐positive sera in normal human serum (NHS) or newborn calf serum (NCS); sera diluted in NHS showed a significant increase in titre, particularly IgM ACA‐positive sera. This phenomenon was found to be due to a serum cardiolipin‐binding cofactor which enhances antibody recognition. The cofactor is heat stable and is present in normal sera (male and female) and also in IgG ACA‐positive sera. The binding of a human IgM monoclonal antibody to cardiolipin was not affected by the cofactor. The cardiolipin/cofactor complex may represent the optimal autoantigen/autoimmunogen and are‐appraisal, therefore, of the clinical relevance of antibodies to cardiolipin and other negatively charged molecules is warranted.

ISSN:0004-945X    

DOI:10.1038/icb.1991.4

出版商:Blackwell Publishing Ltd    

年代:2017

数据来源: WILEY

摘要:

SummaryIn this paper the phenomenon of suppression of proliferationin vitroof 14 day primed, West Nile Virus (WNV)‐specific, murine CD4+T cells by large numbers of antigen‐presenting macrophages and B cells has been investigated. Suppression was apparently not mediated by prostaglandins, as the use of indomethacin in cultures at four times the usual concentration did not reverse suppression.Experiments were designed to evaluate the contribution of major histocompatibility complex (MHC) Class II and nominal WNV antigens in causing suppression of T cell proliferation.Listeria‐ or thioglycollate‐induced macrophages from CBA/H (H‐2k) mice, when treated with heat‐killedListeria in vitrofor 1 h to maintain or increase, respectively, MHC Class II levels before the addition of alloreactive Iak‐specific T cells caused inverse dose‐responses; the highest T cell proliferation occurred at a stimulator to responder (S:R) ratio of 0.25 and profound suppression at a S: R ratio of 1 or 2. In contrast, untreated thioglycollate‐induced macrophages, which express low MHC Class II levels, gave a direct dose‐response with increasing T cell proliferation as antigen‐presenting cell (APC) numbers increased.Addition of anti‐Ia antibodies (or their Fab fragments) to cultures caused a significant reversal of suppresion of anti‐WNV T cells imposed by high numbers ofListeria‐induced macrophages or 14 day WNV‐primed B cell APC. Suppression was also reversed by reducing the concentration of WNV antigen. These observations support the notion that the suppression of T cell proliferation observed at high S: R ratios was due to high concentrations of ligand (WNV‐derived peptide complexed with Class II MHC) on APC.

ISSN:0004-945X    

DOI:10.1038/icb.1991.5

出版商:Blackwell Publishing Ltd    

年代:2017

数据来源: WILEY

摘要:

SummaryIn peripheral lymphoid organs the number of lymphocytes and the proportion of functional lymphocyte subsets are regulated by multiple factors including the control of lymphocyte migration by selective lymphocyte‐high endothelial venule (HEV) interactions. In this study, prostaglandin E2(PGE2) levels from normal and autoimmune mouse lymph node cells were measured. The contribution of eicosanoids to lymphocyte‐HEV interactions in normal (CBA/T6) and autoimmune (MRL/n) mice was examined. There was no association between PGE2production in normal or autoimmune mice and the age of onset of disease activity in the latter strains. Arachidonic acid metabolites, in particular PGE2and leukotriene B4(LTB4), did not have any effects on lymphocyte‐HEV binding. Likewise, lymphocytes treatedin vivoand/orin vitrowith arachidonic acid metabolite inhibitors (acetyl salicylic acid, indomethacin, BW755C) did not alter lymphocyte‐HEV binding interactions in both normal and autoimmune mice. No clinical significance could be attributed to lymph node PGE2production and the age of onset of autoimmune disease. In summary, these findings cast doubt on the role of arachidonic acid metabolites in lymphocyte‐HEV binding interactions.

ISSN:0004-945X    

DOI:10.1038/icb.1991.6

出版商:Blackwell Publishing Ltd    

年代:2017

数据来源: WILEY

摘要:

SummaryFive monoclonal antibodies (MoAb) were produced to the envelope (E) protein of Kunjin (KUN) virus. Three of these were specific for the KUN/West Nile complex, and two reacted with epitopes that were common to the flavivirus family. These MoAb defined at least four distinct epitopes on the E protein of KUN virus. Eight MoAb were also produced to unidentified proteins of Kokobera (KOK) virus. Seven were specific for KOK, while the remaining antibody cross‐reacted with Stratford virus and an unregistered flavivirus CS946. The application of these MoAb to arboviral surveillance is discussed.

ISSN:0004-945X    

DOI:10.1038/icb.1991.7

出版商:Blackwell Publishing Ltd    

年代:2017

数据来源: WILEY

摘要:

SummaryColony‐stimulating factors (CSFs) are not only regulators of haemopoiesis but can also enhance the function of mature myeloid cells, and are therefore potential immune adjuvants. By use of the polymerase chain reaction (PCR) with primers based on the bovine granulocyte‐macrophage CSF (GM‐CSF) sequence, we have amplified the cDNA for ovine GM‐CSF, produced from crude mRNA extracted from alveolar macrophages. The PCR product was cloned into pUC 119, and electroporated intoEscherichia coli.The complete nucleotide sequence of two clones, and the partial sequence of eight others, was determined. At the nucleotide and amino acid levels, the ovine and bovine GM‐CSF sequences are 91% and 81% homologous, respectively.

ISSN:0004-945X    

DOI:10.1038/icb.1991.8

出版商:Blackwell Publishing Ltd    

年代:2017

数据来源: WILEY

ISSN:0004-945X    

DOI:10.1038/icb.1991.9

出版商:Blackwell Publishing Ltd    

年代:2017

数据来源: WILEY

摘要:

Book review in this articlePLATELET ACTIVATING FACTOR AND HUMAN DISEASEEdited by P. J. Barnes, C. P. Page and P. M. Henson.DISEASE AND SOCIETY: A RESOURCE BOOKCompiled by Ruth Dircks.

ISSN:0004-945X    

DOI:10.1038/icb.1991.10

出版商:Blackwell Publishing Ltd    

年代:2017

数据来源: WILEY