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Journal of Leukocyte Biology | 1994

Chemokine expression in trinitrochlorobenzene-mediated contact hypersensitivity

Subhash C. Gautam; Jack R. Battisto; Jennifer Major; David Armstrong; Mark H. Stoler; Thomas A. Hamilton

The expression of the murine IP‐10 and MCP‐1 genes has been examined in the skin of mice during contact hypersensitivity reactions to the hapten trinitrochlorobenezene (TNCB). In both naive and passively sensitized animals, challenge with TNCB resulted in elevated expression of both genes as early as 4 h as detected by Northern hybridization analysis. Twenty‐four hours after challenge, expression was markedly reduced in naive animals but remained elevated in sensitized animals. This prolonged expression of chemokine gene products correlates with the tissue swelling response generally used as a measure of delayed‐type hypersensitivity (DTH) in this model and suggests that the continued expression of these genes results from the stimulation of hapten‐specific T helper cells. Examination of cell type expression patterns by in situ hybridization using 3H‐radiolabeled riboprobes confirmed the results of Northern hybridization experiments. Both genes were expressed predominantly in cells exhibiting the morphology of connective tissue fibroblasts, although the distribution of cells positive for IP‐10 mRNA expression differed from that of cells expressing MCP‐1 mRNA. IP‐10 expression was localized almost exclusively to a population of connective tissue cells surrounding the fur follicle. MCP‐1 expression was rarely found associated with fur follicles but instead was distributed throughout the dermis in cells embedded in the collagenous extracellular matrix. Surprisingly, neither endothelial cells lining the small vessels located deep within the dermis nor epidermal keratinocytes were positive under any of the conditions utilized in the present study. Expression of both IP‐10 and MCP‐1 has been previously reported in a variety of distinct cell types in vitro. The present results indicate that only a subset of the cell types with such potential are stimulated to express these chemokine genes in vivo during hapten‐mediated DTH responses, implying the presence of subtle cell type‐ and tissue‐specific control mechanisms. J. Leukoc. Biol. 55: 452–460; 1994.


Cellular Immunology | 1991

L3T4 (CD4+) cells that mediate contact sensitivity to trinitrochlorobenzene express I-A determinants

Subhash C. Gautam; James A. Matriano; Nathaniel F. Chikkala; Mark Edinger; Raymond R. Tubbs

The present study has further characterized the T cell-mediated inflammatory response of contact sensitivity (CS) to the hapten trinitrochlorobenzene (TNCB) in mice. A discernible CS response was found to be induced as early as 2 days after epicutaneous application of TNCB. The response peaked on Days 4 to 5 and it then declined to a nearly undetectable level by Days 10 to 11. Examination of the draining lymph nodes demonstrated that development of CS coincided with an increase in cellular proliferation and in the total number of cells present. Despite a severalfold increase in the cellular contents of the draining lymph nodes of sensitized mice, the relative percentages of most subsets of T cells remained unchanged. Flow cytometric studies revealed that the subpopulation of T cells characterized as Thy 1.2+ L3T4+ I-A+ increased substantially in comparison to its presence in unsensitized mice. Whether the Thy 1.2+ L3T4+ I-A+ cells that increased following sensitization represented the effector population that mediates CS was then examined. Four-day immune lymph node T cells or L3T4 cells positively selected from them were capable of adoptively transferring CS to normal mice. However, these cells, after treatment with anti-Ia antibody or anti-I-A monoclonal antibody and complement, were unable to transfer CS. These findings imply that expression of I-A determinants may indicate antigen-induced T cell activation in vivo and that L3T4 cells that mediate CS are I-A positive.


Cellular Immunology | 1982

Control of suppressor cell activity: Autoanti-idiotype B cells produced by painting with picryl chloride inhibit the T-suppressor cell which blocks the efferent stage of contact sensitivity

Geoffrey L. Asherson; Marek Zembala; Subhash C. Gautam; Madeleine C. Watkins

Abstract This paper describes a B “suppressor of suppressor” cell which blocks the production or action of the T-suppressor cell, Ts-eff (cs), which acts at the efferent stage of the contact sensitivity reaction. Ts-eff (cs) occur in mice 7 days after injecting picrylsulfonic acid (PSA) and are assayed by their ability to block the passive transfer of contact sensitivity in a 24-hr experiment. These Ts-eff (cs) cannot be demonstrated in mice painted with picryl chloride and injected with PSA 8 days later. In fact, 8 days after painting mice contain B cells which prevent the appearance of Ts-eff (cs) following the injection of PSA. Moreover, the serum of mice 12 days after painting contains antibody which inactivates Ts-eff (cs). This antibody is anti-idiotypic as shown by its absorption to and elution from insolubilized mouse anti-picryl antibody and the lack of effect of absorption with insolubilized picryl groups. The antibody belongs to the IgG2a class and requires an intact Fc moiety for its action.


Cellular Immunology | 1983

Suppression of contact sensitivity and cell-mediated lympholysis by oral administration of hapten is caused by different mechanisms

Subhash C. Gautam; Jack R. Battisto

Oral administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS), a water-soluble analog of trinitrochlorobenzene (TNCB), causes suppression of contact sensitivity (CS) to picryl chloride. We wished to determine what effect oral administration of TNBS (10mg), 10-12 days prior to sensitization, caused significant suppression of CS to picryl chloride. However, mice had to be fed at least three times at weekly intervals to cause suppression of the CTL response. CS was inhibited both at the afferent (induction) as well as at the efferent (effector) phase of the response. The unresponsiveness for CS was readily transferrable with cells from spleen, Peyers patches, and mesenteric lymph node cells from fed mice. In contrast, although the hapten specific CTL response was significantly suppressed in mice fed three times. suppression could not be transferred with any of the aforementioned lymphoid populations. Furthermore, spleen cells from fed mice showed a significantly enhanced in vitro CTL response after stimulation with hapten-modified syngeneic stimulator cells. The results indicate that suppression of CS and of the CTL response in TNBS fed mice is probably caused by different mechanisms.


Journal of General Virology | 1992

Restricted replication of vesicular stomatitis virus in T lymphocytes is coincident with a deficiency in a cellular protein kinase required for viral transcription

David E. Sleat; Nathaniel F. Chikkala; Subhash C. Gautam; Amiya K. Banerjee

Vesicular stomatitis virus (VSV) fails to replicate in mouse T lymphocytes unless the cells have been mitogenically stimulated with concanavalin A (Con A). We have examined the possibility that the failure of VSV to replicate in unstimulated T lymphocytes can be attributed to a deficiency in a host protein kinase which activates the viral P protein by phosphorylation, thus rendering it transcriptionally competent. Soluble extracts were prepared from purified mouse T lymphocytes, with or without prior treatment with Con A. The ability of these extracts to phosphorylate bacterially synthesized P protein of two VSV serotypes was measured in vitro. Activity of the protein kinase on the P proteins of the Indiana or New Jersey serotypes of VSV increased, on average 2.4- and 2.1-fold respectively, after treatment of the cells with 3 micrograms/ml Con A. Higher concentrations of Con A induced proportional increases (up to 10-fold) in the activity of the host protein kinase. Activities of the kinase phosphorylating the P protein in separate populations of CD4- and CD8-containing murine T lymphocytes increased similarly on mitogenic activation. No biochemical or immunological differences were observed between the T cell protein kinase and the previously characterized protein kinase (casein kinase II) from BHK-21 cells. The activity of the kinase that phosphorylates the P protein did not vary in CV-1 cells on treatment with alpha- or gamma-interferon, both of which inhibited VSV replication. Similarly, casein kinase II activities in Raji and SIRC cells, which do not normally support VSV growth, were the same as in BHK-21 cells. Thus restriction of VSV replication in these cells, in contrast to T lymphocytes, was not associated with a deficiency in the host casein kinase II activity.


Cellular Immunology | 1984

Characterization of two suppressor cells that together prevent in vivo development of cytolytic T cells to hapten-altered self

Subhash C. Gautam; Karla D. Beckman; Henry L. Wong; Jack R. Battisto

Two suppressor cell populations that interact to down-regulate in vivo development of the cytolytic T-cell (CTL) response to trinitrophenyl-modified syngeneic spleen cells (TNP-SC) have been further characterized. Suppressor cells induced by the iv injection of trinitrophenyl-modified syngeneic spleen cells possess Thy 1.2 antigen. Their precursors are insensitive to pretreatment of host animals with cyclophosphamide (CY). Suppressor cells that arise after dermal sensitization with trinitrochlorobenzene are also Thy 1.2 antigen positive but their precursors are sensitive to pretreatment with CY. These characteristics of the two suppressor T cells (Ts) are identical to those of the two Ts that are generated by similar methodologies and that together suppress contact sensitivity (CS) to picryl chloride. Neither the CS nor CTL response was suppressed when host animals possessed only one set of Ts. In contrast to suppression of CS at the efferent phase, development of CTL was suppressed only when the two Ts were present early during sensitization (afferent phase). Since the results point to several similarities between the two sets of Ts that are active in the down-regulation of the CS and CTL responses, it is suggested that the two dissimilar immune responses directed to the same hapten, namely CS and CTL, may be controlled by the same suppressor cells. Since it appears that the two sets of Ts interact to affect different phases of the CS and CTL responses, down-regulation of each must be accomplished through different mechanisms.


Cellular Immunology | 1986

Natural cytotoxic T cells (NCTC) that differ from natural killer (NK) and natural cytotoxic (NC) cells are present in Peyer's patches of mice

Subhash C. Gautam; Karla D. Beckman; Jack R. Battisto

We have examined noninduced cytotoxicity of mouse gut associated and peripheral lymphoid tissues for a wide variety of syngeneic as well as allogeneic cell lines and lymphoblasts. Lymphoid cells from Peyers patches were found to lyse these targets in a 3-hr chromium release assay whereas lymphoid cells from intestinal mucosa, mesenteric or peripheral lymph nodes, spleen, and thymus did not. The variety of targets toward which Peyers patch cells were cytotoxic established the latter as nonspecific and H-2 unrestricted. The cell responsible for the lytic event was identified as possessing Thy 1.2 and Ia surface antigens. This naturally cytotoxic T cell (NCTC) was found to be adherent to nylon-wool but not to plastic plates. Although both natural killer cell (NK) and non-NK targets served as targets for the NCTC, the latter were further differentiable from NK cells by lack of asialo GM1 surface marker, which is present on NK cells. In addition, NCTC remained fully functional in mice given either of the drugs cyclophosphamide or cortisone. Each of these drugs, in the doses used, markedly reduced poly(I:C)-induced NK activity. Thus, NCTC differs from NK on the basis of the spectrum of targets against which it is functional, phenotypic surface markers, insusceptibility to stimulation with poly(I:C), and insensitivity to diminution by the immunosuppressive drugs cyclophosphamide and hydrocortisone. Since NCTC is a Thy 1.2 antigen-bearing cell and is detectable in a 3-hr cytotoxic assay, it also differs from the natural cytotoxic (NC) cell. NC lacks the Thy 1.2 marker and becomes detectable only in an 18-hr cytotoxic assay. Thus, NCTC is neither an NK nor an NC cell. We have discussed the possibility that the three naturally occurring cells may be related by being dedifferentiated descendants of an antigen-specific cytotoxic T lymphocyte (CTL). Alternatively, since NCTC is confined to an anatomical site prone to ample antigenic exposure and is still identifiable as a T cell, it may be in linear transition from the CTL to the NK or NC stages.


Cellular Immunology | 1991

Differences in murine gut-associated lymphoid tissues in generating broadly nonspecific cytotoxic cells in response to interferon α AD and interleukin 2

Nathaniel F. Chikkala; Subhash C. Gautam

We examined the response of cells of murine gut-associated lymphoid tissues to agents that augment the activity of natural killer (NK) cells. Specifically, we studied the effect of polyinosinic: polycytidylic acid (Poly I:C) in vivo, and recombinant interferon alpha A/D (rIFN alpha A/D) and recombinant interleukin 2 (rIL2) in vitro on lymphoid cells of mesenteric lymph nodes (MLN) and Peyers patches (PP) in generating cytotoxicity against NK-sensitive (YAC-1) and NK-insensitive (B16BL6) tumor targets. The effect of these agents on spleen cells was examined for comparison with their effect on MLN and PP cells and as a positive control. MLN and PP cells lacked spontaneous NK activity: however, NK activity could be augmented to different levels by the three agents. The treatment of mice in vivo with Poly I:C induced considerable cytotoxicity in the spleen and MLN but only a weak cytotoxic response in PP. The in vitro enhancement of NK activity by rIFN alpha A/D was strong in the spleen, intermediate in MLN, and consistently poor in PP. The weak NK augmentation by rIFN alpha A/D in PP was not restricted to a single mouse strain. PP cells from five strains of mice responded poorly to rIFN alpha A/D. Furthermore, NK augmentation by rIFN alpha A/D in PP cells did not improve after passing the responder cells through nylon wool, indicating that the lack of augmentation of NK activity was not the result of a preponderance of B cells or the masking of NK cells by adherent lymphoid populations in PP. In contrast to weak augmentation of NK activity by rIFN alpha A/D, considerable IL2-induced lymphocyte-activated killer (LAK) activity against NK-insensitive B16BL6 tumor cells was induced in PP. Limiting-dilution analysis showed that the frequency of LAK precursors in the MLN and PP was not markedly different from that of the spleen. The differences among spleen, MLN, and PP lymphoid populations in generating the broadly nonspecific cytotoxic effector cells in response to rIFN alpha A/D or rIL2 may result from differences in the pools of different pre-NK cells or to differential sensitivity of the same pool of pre-NK cells to rIFN alpha A/D and rIL2 in different anatomical locations.


Journal of Immunology | 1992

IL-4 suppresses cytokine gene expression induced by IFN-gamma and/or IL-2 in murine peritoneal macrophages.

Subhash C. Gautam; Julie M. Tebo; Thomas A. Hamilton


Journal of Immunology | 1983

Two distinct suppressor T cells acting in concert cause suppression of cytolytic T lymphocyte (CTL) response to hapten-altered self in vivo.

Subhash C. Gautam; K D Beckman; H L Wong; Jack R. Battisto

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