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J Puri

Publications and source records attributed to J Puri.

35 records · Page 2Linked to original sources
PubMed1990

Functional consequences of phospholipase A2 activation in human monocytes.

Human monocytes release arachidonic acid upon stimulation with a variety of soluble or particulate agents. These include: phorbol esters (i.e., 12-O-tetradecanoate phorbol-13-acetate, TPA), calcium ionophores (ionomycin), serum-treated zymosan (STZ) concanavalin A (Con A), and, to a minor degree, lipopolysaccharides (LPS). Protein Kinase C activation or increased intracellular Ca2+ are common features of the actions of most, if not all, of these stimuli. Prevention of PKC activation by the use of staurosporine or chelation of extracellular calcium by EGTA selectively impaired AA release, indicating that PLA2 may be regulated by either pathway concurrently. The generation of inositol phosphates and diacylglycerol by the action of phospholipase C, notably upon interaction with opsonized particles during phagocytosis, apparently constitutes the physiological correlate of stimulation via these agents. Release of arachidonic acid by the action of PLA2 or other phospholipid hydrolyzing enzymes leads directly to the formation of cyclooxygenase products. In the presence of markedly elevated calcium concentrations, 5-lipoxygenase (LO) is activated as well, leading to the formation and release of leukotrienes. Agents which stimulate AA release also initiate other monocyte functions, including generation of reactive oxygen intermediates and lymphokine release. This observation makes it tempting to implicate PLA2 activation in many aspects of monocyte physiology. However, no correlation with PLA2 activation and either superoxide or lymphokine release was found when multiple stimuli, including TPA, ionomycin, serum-treated zymosan, concanavalin A, or LPS, were compared simultaneously. Instead, our results indicate that PLA2 activation is regulated by the same mechanisms, including PKC activation and increased Ca2+, as are other enzymes which determine expression of monocyte function. Phospholipase A2 (PLA2) hydrolyzes fatty acid from the sn-2 position of a wide variety of phospholipids. Substrates for this (these) enzyme(s) include species which contain a variety of polar head groups (choline, serine, ethanolamine, etc.) and some phospholipids with either linkages in sn-1. In many cell types, including human monocytes, phospholipase A2 commonly acts on substrates containing arachidonic acid (AA). The liberation of free arachidonate is a first step in the metabolism of prostaglandins, hydroxyeicosatetraeinoic acids, (HETE'S), and leukotrienes (Lt's). Monocytes and macrophages have been shown to be rich sources of arachidonate and its metabolites. Some biologic properties of monocytes, notably their role as immunomodulating cells, have been attributed to eicosanoid production and release. Accordingly, much of the interest regarding PLA2 in human monocytes centers on this aspect of their function.(ABSTRACT TRUNCATED AT 400 WORDS)

Arachidonic Acid↗
PubMed1989

Genetic control of immune response to a purified Schistosoma mansoni antigen. I. Effect of MHC class II antigens on the cellular, humoral and protective responses.

The influence of the I region of the major histocompatibility complex (MHC) on T-dependent immune responses against a purified schistosome antigen (9B antigen) was investigated. H-2 congenic mice expressing both I-A and I-E antigens (I-E+) showed a higher in-vitro proliferation to 9B antigen as compared to the recombinant strains expressing only I-A (I-E-). These two strains of mice differed both qualitatively and quantitatively in the humoral responses elicited by the purified antigen. Furthermore, in-vivo protection experiments showed that mice which do not express I-E molecules can be partially protected against the disease by prior immunization with the 9B antigen in contrast to their I-E expressing counterparts. The possible role of the I-E molecule in the immune responses elicited during Schistosoma mansoni infection is discussed.

Animals↗
PubMed1989

Genetic control of immune response to a purified Schistosoma mansoni antigen. II. Establishment and characterization of specific I-A and I-E restricted T-cell clones.

T-cell lines and clones specific for a partially protective schistosome antigen (9B antigen) were established from mice immunized with such antigen. The H-2 congenic strains B10.A which express both I-A and I-E class II gene products of the major histocompatibility complex (MHC) and B10.A(4R) which only express I-A molecules were used in these studies. The specific T-cell lines recognized the 9B antigen in the context of either A or E molecules, but both class II antigens were necessary for maximal stimulation of the T-cell lines in lymphocyte proliferation assays. T-cell clones were derived from these lines and their MHC restriction was investigated. Both I-A and I-E restricted clones could be isolated. All clones were specific for 9B antigen showing different degrees of cross-reactivity with a total schistosome extract (CA sonicate). A correlation between the fine specificity of the clones and the expression of class II antigens was demonstrated. Clones specific for 9B antigen, or which reacted to the same extent with 9B antigen and CA sonicate, were I-A restricted, whereas clones which proliferated more in the presence of CA sonicate were all I-E restricted. This suggests that I-E restricted clones recognize more cross-reactive epitopes than I-A restricted clones. These antigen-specific T-cell clones should provide a useful tool for examining the role of class II antigens in the modulation of protective immune response during Schistosoma mansoni infection.

Animals↗
PubMed1988

Selective inhibition of antigen presentation to cloned T cells by protease inhibitors.

The effect of eight microbial protease inhibitors on Ag-presentation to six different Ag-specific T cell clones was investigated. We found that these protease inhibitors can inhibit Ag presentation in a highly selective manner. This selectivity was evident with T cell clones specific to different Ag as well as with T cells specific to the same Ag but differing in their H-2 restriction. The inhibition was to due to cytotoxicity or effects through the TCR because none of the eight inhibitors inhibited IL-2-induced T cell proliferation, and because they did not inhibit Ag presentation by fixed APC or synthetic polypeptide. The conclusion after these data suggests that each specific antigenic fragment is produced by a unique set of proteases.

Animals↗
PubMed1987

Induction of interferon-gamma production and Ia expression by interleukin 1 in bone marrow culture cells.

Colony-stimulating factor-induced bone marrow (BM) cultures are a good source of antigen-presenting macrophages. However, they failed to present antigen to T cell clones when antigen was introduced as a short pulse only. Adding interleukin 1 (IL1) to BM culture cells before antigen pulse restored their antigen-presenting activity concomitant to a 2-10-fold increase in Ia antigenicity. We performed a series of experiments to test the mechanism of this IL1-induced activation. Our findings suggest that IL1 influences Ia expression and antigen-specific T cell proliferation by inducing interferon-gamma (IFN-gamma) production. IFN-gamma is produced in this system probably by residual Thy-1-positive cells in the BM cell culture.

Animals↗
PubMed1986

Antigen-Ia interaction and the proteolytic processing of antigen: the structure of the antigen determines its restriction to the A or E molecule of the major histocompatibility complex.

The effect of a protease inhibitor, leupeptin, on the presentation of hen egg lysozyme (HEL) to cloned T cells was investigated. We found that leupeptin-sensitive thiol proteases are apparently less involved when HEL is presented by the I-Ad molecule, than when it is presented by the I-Ed molecule. This selectivity was more of a function of the antigen than that of the Ia molecule because presentation of denatured or fragmented HEL was not sensitive to leupeptin whereas antigen presentation to a number of I-A-restricted T cell clones specific to other antigens was sensitive to leupeptin. These data demonstrate that the particular combination of major histocompatibility complex/nominal antigen recognized by a certain T cell clone may require processing of the antigen molecule through a certain group of proteases and that other combinations are independent of that particular processing pathway. Furthermore, there is a preference for a certain type of processing depending on the Ia molecule involved.

Animals↗
PubMed1985

Antigen processing by macrophages: definition of the ligand recognized by T-inducer cells.

An interaction between antigen and macrophage-like cells which display I region gene products [antigen-presenting cells (APC)] is necessary for activation of inducer T cell clones. The specificity of inducer cell activation has been found to be major histocompatibility complex (MHC)-restricted and antigen specific. This is thought to reflect formation of a ligand consisting of MHC class II gene products associated in some way with foreign protein. A panel of inducer T cell clones with different activation specificities and homogeneous lines of APC expressing different MHC haplotypes was used to define this ligand. We isolated a product formed after interaction between antigen and APC expressing defined MHC products. This ligand binds only to the T cell clones that are specifically activated by the same antigen and APC as judged by tritiated thymidine incorporation. The ligand is composed of two moieties: I-A determinants and the foreign protein ("antigen"). Coelution and sequential precipitation studies of the two moieties indicate that the nominal antigen and MHC product are tightly linked. The implications of these findings are discussed.

Animals↗
PubMed1981

Two separate genes regulate self-Ia and carrier recognition in H-2-restricted helper factors secreted by hybridoma cells.

H-2 heterologous T cell hybridomas were used to study the genetic control of dual, anti-nominal antigen and anti-self H-2 specificity of H-2 restricted T cell factors. Each of four hybridoma clones produced two helper factors. One was restricted for the Ia type of the normal T cell partner (H-2b), whereas the other was restricted for the ia type of the lymphoma partner (H-2k) of the somatic hybrid. This was shown by affinity separation on parental type spleen cells and on monoclonal anti-I-A-Sepharose. Both factors had carrier (chicken gamma globulin; CGG)-specific helper effect, and both bound to anti-VH-315-Sepharose. Because the lymphoma (BW-5147) partner could not contribute a CGG-specific locus, the H-2k-restricted, CGG-specific factor had to be the product of segregating anti-nominal and anti-self loci. This suggests that dual specificity is due to two independent loci and support the validity of dual recognition concepts. Anti-self specificity was associated with homologous Ia alloantigens in the individual factors. Therefore, Ia and anti-self might be linked. Implications of the major histocompatibility complex or VH nature of anti-self receptors and the relationship of T cell factors and receptors was discussed.

Animals↗
PubMed1981

H-2-restricted helper factor secreted by clone hybridoma cells.

Biological and serological characteristics of a helper factor secreted by cloned hybridoma cells was described. The factor is carrier specific and contains determinants shared with immunoglobulin VH bu does not react with V kappa- or V lambda-specific antibodies. Presence of four H-2I-controlled antigenic specificities, Ia.ml, Ia.m2, Ia.17, and Ia.m7, was detected. Hence, it is possible that both A beta and E alpha loci may be involved in its control. Helper effect could be obtained only toward B cell sources that shared the H-2K and I-A antigens with the hybridoma cells. Similarly, the factor was absorbed only by spleen cells syngeneic in I-A. Previous studies have demonstrated that this clone binds antigen in an H-2-restricted manner. It follows that H-2-restricted helper cells produce H-2-restricted helper factors. Hence, they support the view that specific T cell factors may represent secreted T cell receptors.

Animals↗
PubMed1981

Specificity of antigen binding by T cells; competition between soluble and Ia-associated antigen.

Competitive antigen binding experiments were performed with purified T and B cells of C3H.SW (H-2b) mice. As antigen, (T,G)-A--L [poly-L(Tyr,Glu)-poly-DL-ALa-poly-L Lys] was used, both in an Ia-containing form, released by adherent cells (IAC-Puri and Lonai, Eur. J. Immunol. 1980. 10:273), and in regular solution. It was found that regular (T,G)-A-L did not compete with the binding of 125I-labeled-IAC-(T,G)-A--L even at a 10(4)-fold excess, whereas IAC-(T,G)-A--L inhibited binding at 10-fold excess. The specificity of (T,G)-A--L binding to high-responder T and B cells was compared by using related branched synthetic copolymers as competitors. B cells cross-reacted with (T,G)-A--L, (H,G)-A--L, (G)-A--L and (T,G)-Pro--L. In contrast, antigen binding C3H.SW T cells cross-reacted only with (T,G)-A--L and (Phe, G)-A--L to both of which they are Ir gene-controlled high responders. Evidence for the Ir gene control of IAC-binding T cells was obtained by showing that high X low responder F1 hybrid T cells preferentally bind IAC-(T,G)-A--L processed by processor cells deriving from the high-responder parental strain. These data are interpreted to suggest that T cells have high affinity for antigen plus self Ia complexes, whereas they have a much lower, if any, affinity for free antigen. It also follows from the results that the structure of the complex ligand may have a role in defining the specificity, H-2 restriction and Ir gene control of T cells.

Animals↗
PubMed1981

H-2-restricted antigen binding by a hybridoma clone that produces antigen-specific helper factor.

Somatic cell hybrids were prepared by fusing the AKR mouse lymphoma BW-5147 with splenic T cells from mice immunized with 4-hydroxy-3-nitrophenylacetic acid (NP) conjugated to chicken serum globulin (CG). From 500 fusion lines 11 were selected on the basis of binding radioiodinated NP-CG. The autoradiographic binding assay was based on previous findings which showed that Lyt-1+ T cells need a lymphokine, lymphocyte-activating factor (LAF), for optimal antigen binding and that they bind preferentially a self-Ia-associated antigen complex, IAC, which is released by adherent cells upon incubation with antigen. Six of the 11 antigen-binding positive lines were tested for helper activity and specific helper factor production in vitro. All of them were found to be positive. One clone was characterized in more detail. It secretes a CG-specific helper factor that contains immunoglobulin heavy chain variable region and I-A determinants. The hybridoma cells bind Ia-containing CG complexes specifically. For binding they need to be treated with LAF, and the binding is restricted to syngenicity in H-2 between the adherent cells used to produce IAC and the antigen-binding hybridoma cells. Regular CG does not bind significantly and does not compete even at high excess with the binding of CG-IAC. These data are interpreted to suggest that the antigen is bound by cells of a clone functional helper T-cell hybridoma line in conjunction with products controlled by H-2I and that the receptor of these cells may have considerably higher affinity for Ia-associated than for regular antigen.

Animals↗
PubMed1980

Antibodies to immunoglobulin heavy chain variable regions protect helper cells from specific suicide by radiolabeled antigen.

The antigen-binding receptor of helper T cells was studied by radioactive antigen-caused suicide in vitro. Purified antibodies to immunoglobulin variable regions, obtained from sera of rabbits immunized with isolated VH and VL fragments of mouse myeloma proteins (MOPC 315, XRPC 25), were used to inhibit the binding of radiotoxic antigen. Anti-VH, but not anti-V lambda or anti-V chi inhibited suicide of carrier-primed cells.

Antibodies, Anti-Idiotypic↗
PubMed1977

Abnormal Stomatal Behavior and Hormonal Imbalance in flacca, a Wilty Mutant of Tomato: IV. Effect of Abscisic Acid and Water Content on RNase Activity and RNA.

Plants of the wilty tomato (Lycopersicum esculentum) mutant, flacca, and of the normal cultivar Rheinlands Ruhm growing under either "normal" or high humidity were used in this research. Under normal humidity, RNase activity was much higher in mutant plants in which abscisic acid (ABA) and water content were lower than in the normal plant. The mutant also contained less RNA and protein per cell and less soluble RNA relative to ribosomal RNA as compared with the normal genotype. In ABA-treated mutant plants, RNase activity decreased while RNA, protein, the ratio of soluble to ribosomal RNA and water content increased.Under high humidity, RNase activity in mutant plants was decreased, but was still somewhat higher than that in the normal plant, although water saturation deficit was equal in both plant types. Abscisic acid increased RNase activity in the mutant plants. The content of RNA and protein per cell was similar in both types, but the ratio of soluble to ribosomal RNA remained lower in the mutant. In ABA-treated mutant plants, although the content of DNA and RNA per fresh weight was similar to that of control mutant plants, the ratio of RNA to DNA decreased significantly. In addition, ABA caused an increase of the soluble to ribosomal RNA ratio toward the normal value in mutant plants.Contrary to ABA, kinetin increased RNase activity in the mutant under normal humidity and decreased it under high humidity.A similar incorporation of labeled uridine into RNA in normal, mutant, and ABA-treated mutant plants under normal humidity suggests that the difference between mutant and normal plants in respect to total, soluble, and ribosomal RNA results not from a different rate of RNA synthesis but from a different rate of RNA degradation, i.e. RNase activity.

Journal Article↗
PubMedDate not supplied

Histoplasmosis of the liver: a rare case.

A 39 year old male presented with history of fever and jaundice for 3 months. A liver biopsy showed numerous ovoid fungal bodies around 5 mm in size in the macrophages and Kupffer cells. A diagnosis of hepatic histoplasmosis was made which is an uncommon entity in our country.

Adult↗