bluuebunny/crossref_metadata_2025_split huggingface dataset:
HIV induces modulation of functionally important cellular antigens
Authors: WRIGHTHAM M , SCHIMPF A , PENNINGTON T H , WALKER F , SEWELL H F 
Published: July 2010

SUMMARYInfection of T lymphoblastoid CEM cells with the IIIB isolate of HIV-1 results in modulation of the expression of several cellular antigens in addition to the CD4 molecule. The intercellular adhesion receptor LFA-1 (CD 11 a/CD18) and HLA-DR are markedly induced in the cytoplasm and at the cell surface, and the CD7 antigen is down-regulated, being virtually undetectable by sensitive immunocytochemical techniques in the infected cell population. These modulatory effects are to some degree dependent on the virus isolate examined, as the CBL-1 British isolate did not induce comparable phenotypic changes in the CEM cell line. Furthermore, these effects are not reproduced by recombinant gp120 (MB isolate) or p24 added exogenously to uninfected CEM cells. The CD7 molecule appears to play a regulatory role in T cell proliferation, and the LFA-1 integrin molecule is involved in a wide range of immunologically important cell-cell interactions, as well as HIV-induced syncytium formation. The possible contributions of such effects to the pathogenesis of HI V infection are considered.
A 72-kD B cell-associated surface glycoprotein expressed at high levels in hairy cell leukaemia and plasma cell neoplasms
Authors: PULFORD K , MICKLEM K , THOMAS J , JONES M , MASON D Y 
Published: July 2010

SUMMARYThe present paper describes two new MoAbs, GHI/75 and VMP55, which were raised against a glycoprotein enriched lysate of hairy cell leukaemia. These antibodies recognized a new antigen of 72 kD (unreduced) and 83 kD (reduced) molecular weight. GHI/75 and VMP55 gave very strong staining of plasma cells, moderate labelling of circulating B cells but only weak staining of monocytes, some tissue macrophages and lymphoid cells. Neither antibody reacted with neutrophils or any non-haematopoietic cells. Both antibodies, however, strongly labelled the tumour cells in hairy cell leukaemia, multiple myeloma, plasmacytoma and lymphoplasmacytic lymphomas. No staining was seen of the neoplastic cells in Hodgkin’s disease, myetoid leukaemia or T cell lymphomas. The two antibodies, GHI/75 and VMP55, may be of value in the differential diagnosis of hairy cell leukaemias and plasma cell neoplasms. In addition, the ease with which their antigen can be purified provides the possibility for a detailed study of this molecule.
Pigeon breeders’ lung: pigeon intestinal mucin, an antigen distinct from pigeon IgA
Authors: TODD A , COAN R M , ALLEN A 
Published: July 2010

SUMMARY
Antigens identified by indirect immunofluorescence staining and specific for sera from patients with pigeon breeders’ lung or healthy pigeon breeders, have been isolated from pigeon intestinal mucus. Two antigenic peaks, one pigeon intestinal mucin and the other IgA, were separated by equilibrium centrifugation of water-soluble mucus in B caesium chloride density gradient. Antigenic positive material was identified by a modified double-sandwich ELISA, by inhibition of haemagglutination of turkey erythrocytes and by gel diffusion. Antigenic-positive material co-fractionated on gel-filtration with purified intact and papain digested pigeon mucin, both free of IgA. These studies demonstrate antibodies to two quite different antigens are associated specifically with sera from pigeon breeders, a novel antigen pigeon intestinal mucin and the previously documented pigeon IgA.
The distribution and functional properties of dendritic cells in patients with seronegative arthritis
Authors: STAGG A J , HARDING B , HUGHES R A , KEAT A , KNIGHT S C 
Published: July 2010

SUMMARYDendritic cells (DC), potent antigen-presenting cells, are known to be increased in numbers in inflammatory lesions in rheumatoid arthritis and juvenile chronic arthritis. In this study, patients with seronegative arthritis were studied: the distribution and functional properties of DC enriched low density cells (LDC) from peripheral blood (PB) and synovial fluid (SF) were compared. The composition of LDC from both sources was similar, comprising approximately 30% DC, 60% monocyles with few T lymphocytes. SF was significantly enriched for LDC compared with paired peripheral blood (P&lt;0.0001) or peripheral blood from healthy controls (P &lt; 0.00l). In contrast, patient PB contained fewer LDC (P &lt; 0.05) overall than healthy controls. LDC from both sources were potent stimulators of allogeneic PB T cells in a mixed leucocyte reaction (MLR), but in four out of 10 patients SF LDC were significantly more stimulatory. In autologous MLRs (AMLRs) SF T cells were not stimulated by cither LDC population. This anergy of T cells was confined to the joint as patient PB T cells showed an AMLR response to PB LDC which was similar to that seen in cells from healthy controls. PB T cells also responded to SF LDC; in a minority of patients SF LDC caused significantly greater stimulation in AMLR than PB LDC and the possibility is discussed that this may represent presentation of antigen acquired in vivo.
Genetic studies on experimental autoimmune gastritis induced by neonatal thymectomy using recombinant inbred strains between a high-incidence strain, BALB/c, and a low-incidence strain, DBA/2
Authors: MORI Y , HOSONO M , MURAKAMI K , KATOH H , YOSHIKAWA Y , KURIBAYASHI K , KANNAGI R , SAKAI M , OKUMA M , MASUDA T 
Published: July 2010

SUMMARYThymectomy on day 3 after birth induced autoimmune gastritis (AIG) at the age of 2 months in 51–73% of BALB/c mice, and in only 3–5% of DBA/2 mice. AIG was detected by histological and serological (immunofluorescence staining for detecting anti-parietal cell autoantibody) examination. However, autoantibody was weakly positive in almost all of these DBA/2 mice when measured by ELISA using extract of murine gastric mucosa as the antigen. To investigate genetically the mechanism controlling the incidence of AIG, 11 recombinant inbred strains established by brother-sister mating of (BALB/c x DBA/2) F2 mice (C x D2 strains) were used. Among 26 markers tested, the Mls-1 locus on BALB/c chromosome 1 and the Hc locus coding a complement component (C5) on BALB/c chromosome 2 were found to be associated with high susceptibility to AIG. However, if one or both of the loci were of DBA/2 origin, mice showed medium or low susceptibility to AIG. For further analysis, F1, F2 and back-cross generations of these two strains were tested, but segregation of a single susceptibility or insusceptibility gene was not obtained. Taken together, it seems probable that two or more genes are involved in the induction mechanism of AIG. We did not detect C5 deposition in AIG lesions, nor complement-dependent cytotoxic antibody to parietal cells in serum from AIG mice. However, injection of irradiated spleen cells of DBA/2 mice into BALB/c mice thymectomized on day 3 augmented the incidence of AIG from 71 to 100%, but not that of oophoritis (33%). A relationship between Mls-1a determinants and the pathogenesis of AIG was further suggested from the fact that Vβ6 TcR-expressing T cells increased in number in AIG-bearing compared with normal BALB/c mice.
Intraperitoneal infection withSalmonella abortusovisis partially controlled by a gene closely linked with theItygene
Authors: OSWALD I P , LANTIER F , MOUTIER R , BERTRAND M-F , SKAMENE E 
Published: July 2010

SUMMARYThe aim of the present study was to determine whether the Ity gene, which controls the resistance to S. typhimurium infection in mice, also governs the resistance to S. abortusovis, a serotype specific for goat and sheep. During either i.v. or i.p. infection, BALB/c mice (Itys) were not able to control the growth of S. abortusovis and eventually died from infection. In contrast CBA (Ityr) or (C.CB)F1 (Ityr/s) mice were able to control the growth of these bacteria. Using congenic C.D2 Ityr mice, we found that the gene controlling resistance to S. abortusovis was tightly linked to the Ity gene on chromosome 1. Furthermore, in the spleen and the liver of backcross BALB/c × (CBA × BALB/c) mice, the S. abortusovis resistance phenotype cosegregated with the two alleles of the Len-1 gene, a gene tightly linked to the Ity gene. By contrast, in these backcross mice, the level of infection of the peritoneal cavity, the site of inoculation, did not correlate with the Len-1 phenotype of the animal. These results provide evidence that after i.p. inoculation the control of S. abortusovis growth in the spleen and the liver is controlled by the Ity gene, but also suggest that additional gene(s) regulate the number of bacteria at the site of inoculation.
Gut flora induces and maintains resistance against streptococcal cell wall-induced arthritis in F344 rats
Authors: VAN DEN BROEK M F , VAN BRUGGEN M C J , KOOPMAN J P , HAZENBERG M P , VAN DEN BERG W B 
Published: July 2010

SUMMARY
Streptococcal cell wall (SCW)-induced arthritis is a chronic, erosive polyarthritis that can be induced in susceptible Lewis rats by one i.p. injection of an aqueous, sterile suspension of SCW. F344 rats are resistant to chronic joint inflammation. Our previous studies showed a correlation between susceptibility to SCW-induced arthritis and the ability to mount SCW-specific T cell responses, suggesting tolerance to SCW as a putative mechanism. Here we prevented the induction of tolerance to bacterial epitopes in F344 rats by using them germ-free and analysed susceptibility to arthritis subsequently. In addition, we conventionalized germ-free F344 rats at different times before induction of arthritis. Our results show that germ-free F344 rats are susceptible to SCW-induced arthritis with a similar severity, chronicity, incidence and onset as Lewis rats. Moreover, T cells isolated from germ-free F344 rats were able to respond to SCW. Conventionalization dramatically moderates arthritis and makes T cells unresponsive to SCW again. Thus, in normal rats (F344) a state of tolerance to arthritogenic epitopes is induced (neonatally) and maintained through life by the bacterial flora, resulting in resistance to bacterium-induced artritides. In arthritis-prone (Lewis) rats, this tolerance is deficient and/or easily broken.
IL-2 regulation of soluble IL-2 receptor levels following thermal injury
Authors: TEODORCZYK-INJEYAN J A , SPARKES B G , LALANI S , PETERS W J , MILLS G B 
Published: July 2010

SUMMARYIn the immunosuppresscd burn patient serum levels of both IL-2 and a soluble form of IL-2 receptor alpha (sIL-2Rα) are significantly elevated. Strikingly, the production of these markers by the in vitro activated patients' cells is decreased. This study examines the role of IL-2 in the decreased production of the sIL-2Rαin vitro in patients with major burns (n = 18, 30 to &gt; 70% total body suface area). Peripheral blood mononuclear cell (PBMC) cultures from patients with highly elevated serum sIL-2Rα. and from healthy controls (n = 12) were activated with concanavalin A (Con A) at initiation. In patients' cultures mitogen-induced increments of sIL-2Rα levels were significantly lower. There was a significant negative correlation (r= −0·64, P&lt;0·001) between a high serum sIL-2Rα level and a decreased Iectin-induced sIL-2Rα release in vitro. Low levels of sIL-2Rα in patients' samples were not normalized by increasing the number of T lymphocytes. Also exogenous rIL-1 was without effect. whereas rIL-3 increased sIL-2Rα release in some cultures. However. sIL-2Rα levels were significantly increased in patients' cultures by (i) addition of exogenous IL-2; (ii) removal of adherent cells; (iii) addition of cyclooxygenase inhibitor, indomethacin: (iv) bypassing cell surface activation by the combination of the calcium ionophore A23187 and the phorbol ester 12-o-tetradreanoyl acetate. The cyclic AMP-elevating drug. forskolin. abrogated the ability of exogenous IL-2 to increase sIL-2Rα production. Thus, in the burn patient, the reduced in vitro sIL-2Rα release appears to relate to abnormalities in IL-2 production and action mediated through its functional surface receptor. Elevated levels of sIL-2Rαin vivo may, therefore, reflect systemic activation of T lymphocytes in response to biologically active IL-2.
Immune defects in families and patients with xeroderma pigmentosum and trichothiodystrophy
Authors: MARIANI E , FACCHINI A , HONORATI M C , LALLI E , BERARDESCA E , GHETTI P , MARINONI S , NUZZO F , RICOTTI G C B ASTALDI , STEFANINI M 
Published: July 2010

SUMMARYXeroderma pigmentosum (XP) is a rare autosomal recessive disease characterized by photosensitivity, a high incidence of cancer in sun-exposed portions of the skin and a reduced capacity to repair the u.v. -induced DNA damage. One of the XP mutations (XP-D) has also been identified in patients affected by trichothiodystrophy (TTD), a rare autosomal recessive disease characterized by brittle hair, mental and physical retardation, peculiar face and ichthyosis. However, in these patients there is no evidence of increased skin tumour incidence. Since an impairment of cell-mediated immunity has been proposed as a co-factor in the cancer proneness of XP patients, we investigated the involvement of immune defect(s) in five XP patients, five TTD patients, their parents, and 24 TTD relatives. We evaluated the phenotype of circulating lymphocytes, natural killer (NK) cell lytic activity, target cell binding of NK cells at single cell level and the effect of interferons (IFN)α and β on NK cell activity. The relative proportion of CD3+ and CD4+ circulating lymphocytes was reduced in XP but not in TTD patients. NK cell lytic activity was decreased in XP patients and their mothers, but their fathers showed normal lytic activity. NK activity varied among TTD families: four out of five patients and their relatives presented low NK cell activity, and one family was normal. In TTD family members, NK activity increased after incubation with IFN-α or IFN-β, but never reached normal values. In contrast, in XP patients and their mothers, the defect was almost completely corrected after in vitro incubation with IFN-α or IFN-β. Our study indicates impaired NK lytic activity in the majority of TTD and XP patients and that this defect is present also in members of their families. In addition, XP patients present a low number of circulating T cells. These multiple abnormalities, together with DNA repair defects, could be related to the increased cancer risk in XP patients.
Reduced PMN β2 integrins after trauma: a possible role for colony-stimulating factors
Authors: WHITE-OWEN C , HARTMANN S , ALEXANDER J W , BABCOCK G F 
Published: July 2010

SUMMARYThe β2 inlegrins are composed of a common 95-kD β-subunil (CD 18) and one of three possible α-subunils: CDlla, CDllb, or CD1le, These molecules are involved in neulrophil adhesion, diapodesis, chcmotaxis and phagocytosis. In this study, the effects of traumatic injury on neutrophil expression of these α-subunits were investigated. Neutrophils from patients with severe trauma (n = 30) were stained with fluorescent anti-CDlla, -CD1lb, or -CDlle. The percentage of positive neutrophils and the mean channel fluorescence were assayed by flow cytometry. In 10 patients and 10 normals, the effects ol'granulocyte-colony stimulating factor (G-CSF) and granulocyte-maerophage colony-stimulating factor (GM-CSF) on α–subunit expression were evaluated. Ninety-four .2% (s.e.m.) of normal neutrophils were CDlla+, 89.1% were CDllb4 and 89.8% were CDllc+. Only 65 .2% of patient neutrophils were CDlla+, 45.5% wereCDl lb+ and 8.1% were CDllc+ Culture of normal neutrophils without colony-stimulating factors resulted in reduced expression of CDlla and CDllc, but up–regulation of CDllb. Down–regulation of CDlla and CDllc was partially reversed by colony–stimulating factors (30 U/ml). CD1lb receptor density was further up-regulated by GM–CSF and G–CSF. Treatment of patient neutrophils with colony–stimulating factors in culture resulted in up–rcgulation of a–subunils as well. GM–CSF appeared to have the greater effect. These results indicate that colony–stimulating factors may have a clinical role in improving β2 integrin expression, and suggest a use in these infection–prone patients.
Diagnosis of typhoid fever: detection of Salmonella typhi porins-specific antibodies by inhibition ELISA
Authors: NANDAKUMAR K S , PALANIVEL V , MUTHUKKARUPPAN V R 
Published: July 2010

SUMMARY
Porins are highly immunogenic outer membrane proteins ofSalmonella. Sera from typhoid patients contained a high level of IgG antibodies directed to porins of Salm. typhi. Since porins are highly conserved proteins, anti-porins antibodies both from typhoid patients and healthy normals reacted with porins from several Gram-negative bacteria. Therefore, in order to improve the specificity of detecting Salm. typhi porins-specific antibodies, an inhibition ELISA was developed using enzyme-conjugated MoAbs (MP1 and MPN4) specific to Salm. typhi porins. Sera from typhoid patients with positive haemoculture (16 out of 17) inhibited the binding of MPI to porins, thus showing a positive test for typhoid, whereas sera from patients with other Gram-negative bacterial infections (n= 7) and from healthy volunteers (66 out of 67) were found to be negative. The sensitivity, specificity, accuracy, positive predictive value and negative predictive value of this assay were 94.1, 98.7, 97.8, 94.1 and 98.7% respectively. The validity of our inhibition ELISA for typhoid was higher than that of the Widal test. The diagnosis of typhoid fever as early as 3 days after the onset of fever, using a single specimen is possible.
Study of induction of activation of human peripheral blood mononuclear cells with a non-activating form of anti-CD3 MoAb in autoimmune thyroid disease (AITD)
Authors: RESETKOVA E , ARREAZA G , YOSHIKAWA N , MORITA T , KIM H , CARAYON P , VOLPÉ R 
Published: July 2010

SUMMARYAnti-CD3 (OKT3) MoAb is a mitogenic agent which activates lymphocytes. We have studied the effects of murine anti-human OKT3 MoAb (IgG1) alone or in combination with IL-2. human thyroglobulin (Tg) and thyroperoxidase (TPO) antigens on the proliferation of whole peripheral blood mononuclear cells (PBMC) (including monocytes) or subtypes (T, CD4+, CD8+, B) as measured by tritiated thymidine (3H-TdR) incorporation. B cell differentiation was studied by measuring numbers of IgG-secreting cells and specific anti-TPO/anti-Tg-secreting cells by SPOT ELISA. PBMC or lymphocyte subtypes, obtained from 45 patients with Hashimoto's thyroiditis (HT). 40 Graves’ disease (GD) and 51 normal controls were cultured in 96 microtitre plates for 6 days in the presence of OKT3 MoAb at final concentrations 25–250 ng/ml, IL-2 15 U/ml. Tg and TPO (I νg/ml). Then cultures were pulsed with 0.2 μCi 3H-TdR/well and incorporation was measured after 18 h. IgG and anti-TPO/Tg-secreting cells were detected at 7 days. Higher proliferative responses from whole PBMC preparations in response to any of the combinations including OKT3 MoAb were observed in the HT preparations, while the basal values were the lowest. IL-2 alone increased these responses markedly, but equally in all groups. IL-2 in combination with OKT3 had an additive effect on proliferation, with higher responses in HT. Tg and TPO antigens did not change these responses. Most HT preparations responded with their maximum proliferation to the lowest concentration of OKT3 MoAb (25 ng/ml), whereas in GD and control preparations of PBMC these responses were shifted to higher concentrations (250 ng/ml); even with those, proliferation was not so enhanced in controls when compared with HT and GD preparations. In contrast, the proliferative responses of T cells alone and subpopulations of CD8+ suppressor/cytotoxic cells were decreased in HT preparations compared with controls. Monocytes were necessary for proliferation. In the subpopulation of B cells (&gt; 95% pure) and CD4+ helper/inducer cells, differences did not reach significance. In spite of the effect on proliferation, OKT3 MoAb only mildly but significantly increased the numbers of IgG-secreting cells in HT and GD preparations and did not stimulate synthesis of specific antibodies. Our data suggest that the increased proliferative responses of whole PBMC to OKT3 MoAb in HT preparations might be due to insufficient activation of T suppressor/cytotoxic cells.
Effect of lipoarabinomannan and mycobacteria on tumour necrosis factor production by different populations of murine macrophages
Authors: BRADBURY M G , MORENO C 
Published: July 2010

SUMMARYTumour necrosis factor (TNF) production is an important pathological mediator in mycobacterial infections, and yet little is known of the factors which influence its production. We have studied the influence of murine macrophage heterogeneity and activation state on TNF production following mycobacterial stimulation in vitro. Lipoarabinomannan (LAM) from strains of Mvcobactcrium tuberculosis and Myco, arium differentially stimulated TNF production in thioglycollate-elicited macrophages in a dose-dependent manner. In comparison, resident peritoneal macrophages produced much less TNF when stimulated with LAM. dead mycobacteria or lipopolysaccharide (LPS). In contrast, zymosan stimulated resident macrophages to a higher degree than thioglycollale-elicited cells. Another comparison between bone marrow and thioglycollalc-elicited macrophages showed that both responded to LPS. but only the latter was stimulated significantly by H37Rv LAM. This may indicate that LAM stimulation of macrophages takes place through a different pathway than both zymosan- and LPS-stimulated TNF production. Also, in vitro activation of peritoneal macrophages with interferon-gamma (IFN-γ), increased TNF response to several stimuli. Our studies indicate that the pathology of mycobacterial infections through TNF production may be influenced by the type and activation state of the macrophage which responds to that infection.
The severe combined immunodeficient (SCID) mouse as a model for the study of autoimmune diseases
Authors: VLADUTIU A O 
Published: July 2010

SUMMARYThere are no readily available in vivo models to study immune cells from humans with autoimmune diseases. SCID mice, which virtually lack both T and B lymphocytes and accept xenogeneic cells, have been used during the last 5 years to provide a milieu for lymphocytes isolated from individuals with various autoimmune diseases, or for lymphocytes from mice that have a systemic lupus erythematosus-like syndrome. Whilst human autoantibodies to organ antigens have been demonstrated in most SCID mice engrafted with human lymphocytes from the peripheral blood or the target organ, inflammation of the mouse target organ has not generally been observed. This review critically analyses experiments in this area reported so far. Some pitfalls of the SCID mouse model of human autoimmune diseases are mentioned, and future experiments to study mouse and human autoimmunity with this model are proposed.