ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1992.tb03136.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

SummaryTwo main ideas have been put forward to explain the unexpectedly low anti‐hapten antibody titres which can result from pre‐priming a mouse with carrier before hapten‐carrier immunization. The first involves the interaction of a network of idiotype‐specific suppressor T cells, the second instead arguing for the role of intrinsic B‐cell anergy. This paper proposes that the data available can equally be interpreted as reflecting the suboptimal interaction between T and B cells at differing stages of maturity, provided that memory B cells can be divided into two subsets. Further, it is suggested that these considerations must be taken into account in the analysis of B‐cell anergy in receptor tran

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1992.tb03137.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

The induction of specific effector functions in naive T cells may be directed by accessory signals during activation. These could be elicited through binding to cell surface molecules or through factors secreted by antigen‐presenting cells or other simultaneously activated cells. We have investigated the influence of CD8+cells and of exogenousiy added cytokines (interleukin (IL)‐2, IL‐4 and interferon (IFN)‐γ) on the cylokine production in splenic CD4+T cells. IL‐2, IL‐4, IL‐5 and IFN‐γ production in CD4+cells was measured at the single cell level during primary mitogen stimulation in vitro in the presence or absence of factors or CD8+cells. On day 5 the cells were restimulated with mitogen alone and analysed to evaluate the short‐term development of cytokine‐producing cells in such cultures. Preactivation in the presence of either exogenous IL‐4 or IFN‐γ led to an increased production of IL‐4 and IFN‐γ respectively at restimtilation, and the effects of both IL‐4 and IFN‐γ were augmented by IL‐2. After preactivation in the presence of IL‐2 and IL‐4, every third CD4+cell could be induced to produce IL‐4. Exogenous IL‐4 or IFN‐γ further decreased each other's production. Depletion of CD8+cells before activation resulted in a slight increase of IL‐4‐producing cells, indicating that simultaneous activation of CD8+cells will influence lymphokine production in CD4+cells. The results suggest that the pattern of lymphokines induced in naive cells may be influenced by factors secreted by preactivated CD4+and CD8+cells, and that naive cells are pr

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1992.tb03138.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

The genes located between class II and class I HLA genes including polymorphic tumour necrosis factor (TNF) genes may contribute to the disease susceptibility in IDDM. Restriction fragment polymorphisms of the TNF‐β gene have been found to be fixed in the major IDDM susceptibility haplotypes, the B62,DR4 haplotype being associated with the 10.5‐kb fragment and the B8,DR3 haplotype with a 5.5‐kb fragment. We studied this TNF polymorphism in a sample of diabetic families. In all IDDM‐associated haplotypes (n= 129) the 5.5‐kb allele was more frequent than in haplotypes found only in healthy family members (n=112) (58.1% versus 40.2%, P<0.01). Among IDDM haplotypes the B62,DR4 haplotype was characterized by the 10.5‐kb TNF fragment, whereas two other common Finnish IDDM‐associated DR4 haplotypes‐A24,B39,DR4 and A2,B56,DR4‐had the 5.5‐kb TNF fragment. Both IDDM‐associated and non‐associated DR3 positive haplotypes were linked to the 5.5‐kb fragment. The distribution of various combinations of TNF alleles in IDDM probands (n= 63) did not differ from that expected according to the Hardy‐Weinberg distribution. Our results indicate that the 10.5‐kb allele of TNF‐β gene as such is not a risk factor contributing to DR4/DQ8‐associated susceptibility. Alternatively, there may be heterogeneity

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1992.tb03139.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

We have detected cytoplasmic anti‐Golgi antibody (AGA) during a routine immunofluorescence test for detecting autoantibodies. Two sera from patients with rheumatoid arthritis (RA) reacted to the Golgi complex by an indirect immunofluorescence technique on HEp‐2 cells. Localization of AGA in the Golgi complex was confirmed by double‐staining with antibodies to β‐COP. The effect of monensin on the integrity and morphology of the Golgi complex was also studied. To confirm the presence of AGA further, we performed immuno‐electron microscopy. Both sera reacted with cytoplasmic antigen located in the Golgi complex of various animal tissues. Furthermore, by using the Western blot technique, both sera reacted to a relative molecular weight (MW) of 79 kDa (doublet) Golgi antigen purified from rat liver. To our knowledge, this study may be the first to identify the relative MW of Golgi antigen by the Western blot method. Identification of this antibody could provide better understanding of protein synthesis and secretion. The presence of AGA in RA patients further substantiates the diversified nature of autoantibody production seen in th

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1992.tb03140.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Binding of leucocytes to endothelial cells (EC) is essential as an initial step in inflammatory responses. We present a rapid, non‐radioactive method to measure adhesion of human lymphoid cells to EC using flow cytometry. Freshly isolated peripheral blood mononuclear cells (PBMC) were allowed to adhere to EC grown in 24‐well plates. Non‐adhering cells were removed, after which adhering cells and EC were dissociated using trypsin/EDTA. These samples were subsequently analysed by flow cytometry, using scatter properties to distinguish between adhering cells and EC. The ratio of the number of adhering leucocytes and EC was calculated to quantify adhesion. Results of the flow cytometric adhesion assay were comparable to those obtained with a conventional adhesion assay using chromium‐labelled cells. We additionally show that by using the flow cytometric adhesion assay, adhesion of lymphocyites and monocytes present within the adhering PBMC can be quantified simultaneously. As a model, the contribution of LFA‐1 (CD11a,CD18) and ICAM‐1 (CD54) in adhesion of PBMC to EC was studied. It was found that adhesion of lymphocytes and monocytes is regulated differently by phorbol ester and that the relative contribution of LFA‐1 and ICAM‐1 differs for

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1992.tb03141.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

IgG antibody to gE, the Fcγ‐binding herpes simplex 1 (HSV‐1) viral glycoprotein, was studied in 49 rheumatoid arthritis (RA) patients and 43 normal controls. Antibody to gD, another important HSV‐1 antigen, was assayed in parallel. No difference between RA patients and normal controls was found in levels of anti‐gE antibody measured by reactivity of IgG F(ab')2fragments reacting with gE coated to ELISA plates. No difference in anti‐gD antibody was recorded between normals and patients with RA. Levels of IgG anti‐IgE antibody did not correlate with quantitative elevations of serum rheumatoid factor (RF) in RA patients. When IgG anti‐gE and anti‐gD were assayed in 20 patients with juvenile rheumatoid arthritis and 22 children controls, no significant differences were noted. However, when individual RFs from patients with RA were tested for reactivity against a panel of affinity‐isolated E(ab')2antibodies to gE, some evidence for individual autospecificity was obtained. Four of 20 monoclonal IgM RFs produced from RA patients' B cells showed marked elevations of reactivity with some RA patients'F(ab')2antibodies to gE. All four of the monoclonal RFs showing this specificity were derived from RA synovial tissue B cells. These findings may provide support for the concept that some RFs in patients with RA show individual specificity for internal image determinants of IgG antibodies to viral Fc

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1992.tb03142.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Paratuberculosis (Johne's disease) is a chronic enteritis syndrome of ruminants, which is due to infection byMycobacterium paratuberculosis. Cutaneous testing with proteins extracted from a mycobacterial culture fluid (johnin‐PPD) is currently used to evaluate the cellular immune status. We have compared the components of johnin‐PPD with those of the A36 complex, a thermostable macromolecular antigen (TMA) present in the cytoplasm and associated with the cell wall ofM. paratuberculosis. The presence in the johnin‐PPD of fifteen A36 components has been shown by Western blotting. Moreover, monoclonal antibodies, which bind respectively to the 65‐kDaM. lepraeheat shock protein, the 28‐kDaM. lepraesuperoxide dismutase, andM. tuberculosislipoarabinomannan, recognized components of the johnin‐PPD. The ability of A36 to trigger delayed hypersensitivity reactions in sensitized rabbits, and to induce the proliferation of T lymphocytes from the lymph nodes of A36‐sensitized mice, matched that of johnin‐PPD. The homology levels of T epitopes between A36 and the TMA complexes ofM. phlei, M. bovis, M. tuberculosisandM. aviumwere estimated, in a lymphoproliferation assay, to be 51, 52, 59 and 94% respectively. A strong cross‐reactivity of A36 with anM. lepraesonicate was also observed by cutaneous testing. The A36 components within the 45.2–26.8‐kDa and the 21.6–19.8‐kDa ranges were proved to induce the proliferation of T lymphocytes from sensitized mice. This work supports the possible use of the A36 complex, and of some of its components, for cutaneous tests and lymphocyte proliferation assays, in order to monitor cellular im

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1992.tb03143.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

T lymphocytes isolated from mice infected withMycobacterium tuberculosisrespond vigorously to proteins secreted by the bacilli and these antigens may be of importance in the generation of protective immunity against the disease. In this study, short‐term culture filtrate (ST‐CF), which constitutes a complex mixture of secreted proteins, was fractionated by a modified preparative SDS‐PAGE technique. The ability of each fraction to be recognized by T cells isolated from infected mice was evaluated by quantifying proliferation and IFN‐γ production in cell cultures. Two molecular mass regions 4–11 and 26–35 kDa were found to possess marked stimulatory properties. Four potent single antigens were mapped within the stimulatory regions. These purified antigens stimulated T cells isolated from mice at the height of a tuberculous infection to produce large amounts of IFN‐γ, Two of these stimulatory antigens belonged to lhe ant

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1992.tb03144.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

The aim of this study was to examine the cytokine production and cytokine responsiveness of the first T‐cell receptor (TcR) positive cells that appear in the murine fetal thymus, namely TcR Vγ3 cells. It is shown that IL‐2‐cultured fetal TcR Vγ3 thymocytes were capable of producing IL‐3, GM‐CSF, TNF‐α and IFN‐γ upon TcR triggering. IL‐2, IL‐4, IL‐5 and IL‐6 could not be detected. With regard to cytokine responsiveness, TcR Vγ3 cells proliferated to a high extent when high concentrations of rIL‐2 were added. rIL‐4or rIL‐7 alone, but not rIL‐1 alone, were capable of inducing a modest proliferation of TcR Vγ3 thymocytes. When combined with low concentrations of IL‐2, a synergistic effect could be observed with IL‐1, IL‐4 or IL‐7. It is shown that the synergistic effect of IL‐2 with IL‐4 was mainly due to induction of IL‐2 receptor expression. The synergistic effect of IL‐2 and IL‐7 on the proliferation of TcR Vγ3 cells could only be partially inhibited by anti‐IL‐2 receptor MoAb, and this antibody had no effcet on the IL‐2 + IL‐1 cultures. These observations can explain the extensive proliferation of TcR Vγ3 thymocytes during fetal life and they indicate that TcR Vγ3 thymocytes have the pot

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1992.tb03145.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY