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PubMed1983

Functional reactivities of lymphocytes primed in murine graft-versus-host reactions.

Secondary mixed leukocyte culture (MLC) responses of T lymphocytes effecting graft-versus-host (GVH) reactivity have been compared with the response patterns of T lymphocytes primed in vitro. GVH reactions were initiated in donor-recipient combinations selected to involve genetic differences at the entire H-2 complex or individual K/D and I regions. GVH-primed lymphocytes, whether derived from spleen, liver, or lymph nodes, exhibited unexpectedly specific proliferative reactivity against I region-encoded gene products. In combinations involving both K/D plus I region differences, cytotoxic T lymphocytes were generated against the K/D antigens. These response patterns contrasted to those exhibited by MLC-primed T cells. MLC-primed cells elicited proliferative responses against both K/D and I region antigens and revealed a high cross-reactivity among I region gene products of various haplotypes. The different response patterns for in vivo versus in vitro primed cells do not appear to be artifactual but a result of the priming environment.

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PubMed1983

Reconsideration of the lymphatic drainage of the rat testis.

An extensive investigation of the lymphatic drainage from the rat testis was carried out in an effort to detect any characteristics which might be important in the immunological privilege the testis extends to allografts. Three different methods revealed a consistent and very efficient lymphatic drainage involving primarily the iliac and renal lymph nodes and to a lesser extent the external lumbar, para-aortic, and posterior gastric nodes. Within minutes, dye or labeled cells injected into the testis could be found within regional nodes. Node hypertrophy was induced by injecting the testes of F1 hybrids with parental strain lymphoid cells (a regional graft-versus-host reaction). Besides indicating that efficient filtration occurs in these nodes, this also established that they are a hospitable environment for cellular immune reactions. Similarly, the capacity of allogeneic cells injected into the testis to induce production of humoral alloantibodies by recipients confirms that exposure to antigens via this route does not in itself suppress immune responsiveness.

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PubMed1983

Analysis of neonatally induced tolerance of H-2 alloantigens. III. Ease of abolition of tolerance of class I, but not class II, antigens with infusions of syngeneic, immunocompetent cells.

Neonatally-induced tolerance of class I H-2 alloantigens can be abolished in adult, long-term-tolerant mice by infusions of immunocompetent cells from donors syngeneic with the recipient. By contrast, neonatally-induced tolerance of Ia alloantigens can not be abolished easily, indicating that the Ia-specific tolerant state is maintained by an active process that can be impressed upon mature alloreactive lymphoid cells in the tolerant environment. This finding is concordant with previous observations that tolerance of Ia alloantigens can readily be transferred adoptively by inoculating lymphoid cells from tolerant mice into syngeneic, naive recipients. It is concluded that class II H-2 antigens induce a type of unresponsiveness that class I antigens fail to evoke, an unresponsiveness that is actively maintained among mature immunocompetent cells. It is proposed that, in addition to a central process of clonal deletion/inactivation that both class I and class II H-2 antigens induce in neonatal mice, Ia alloantigens also evoke a secondary, fail-safe mechanism that operates to prevent alloreactivity from emerging when cells with alloreactive potential escape the central mechanism, or mutate to alloreactivity at a later stage of maturation.

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PubMed1983

Specific and nonspecific T-cell-mediated suppression of antihost immune reactivity in graft-versus-host reaction.

Intravenous immunization of mice with irradiated (2000 rads) allogeneic lymphoid cells induces the generation of suppressor T cells. Such suppressor T cells are capable of suppressing the antihost immune reactivity during acute and delayed graft-versus-host reactions. These suppressor T cells are strictly antigen-specific as far as their activation is concerned, but also suppress the reaction against unrelated antigens presented by the irradiated host.

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PubMed1984

Graft-versus-host reactions and abrogation of allotype suppression following histoincompatible lymphoid cell transfers in rabbits.

Noninbred rabbits that were characterized for antigens of the major histocompatibility complex (MHC) by serological (RLA) typing were used as adult donors and newborn recipients of lymphoid cells. The majority of RLA-heterozygous (CE) animals transplanted with homozygous type C cells died before 7 weeks of age with clinical and histological signs of graft-versus-host disease, but a small proportion survived with their lymphoid and erythroid systems completely converted to phenotypes of the donors. Takeover of the host's hematopoietic system was associated with a transient hyperimmunoglobulinemia, mostly of donor origin, and with a striking and permanent abrogation of allotype suppression on the part of donor lymphocytes. In contrast, as shown in this and in earlier publications, recipients of RLA-compatible cells become stable B lymphocyte chimeras without detectable T cells or erythrocytes of donor type. In the latter case allotype suppression is neither established in the recipient nor abrogated in the donor's cells.

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PubMed1985

Generation of mouse cytolytic T cells against human concanavalin A blasts. Involvement of non-MHC determinants in the antihuman response.

Normal human peripheral blood lymphocytes (PBL) are incapable of eliciting a significant murine cytotoxic T cell (CTL) response either in vivo or in vitro. However, using a primary in vivo and secondary in vitro stimulation with lectin-activated PBL, Thy-l-positive cytotoxic cells were produced. The antigens that these T-cells identified were independent of the serum source employed in the culture medium used for lectin activation. The cells always preferentially lysed cells from the immunizing individual but were also able to lyse target cells from unrelated individuals, regardless of HLA identity or disparity with the immunizing individual, suggesting the presence of both a private (possibly class II antigens) and public specificity. Using the lymphoblasts of different family members as immunogen and targets there was slight preference of the CTL for HLA-identical targets with no apparent difference between the lysis exhibited against semiidentical and nonidentical subjects. Monoclonal antibodies directed against HLA DR or beta 2-microglobulin failed to inhibit the cytotoxicity observed in these experiments. It is suggested that under these circumstances of xenogeneic education, non-MHC-restricted T cells may become cytotoxic, and this model may serve as a useful probe to investigate some of the less-well-defined aspects of the T cell repertoire.

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PubMed1985

Characterization of host lymphoid cells in antibody-facilitated bone marrow chimeras.

We have produced stable murine antibody-facilitated (AF) chimeras by the simultaneous injection of P1 bone marrow cells and anti-P2 monoclonal antibody into normal (unirradiated) adult (P1 X P2)F1 recipients. These AF chimeras are healthy, long-lived, and exhibit no overt signs of graft-versus-host disease. They are immunocompetent and tolerant of host, P2-encoded alloantigens. Donor cell engraftment and takeover, monitored by glucosephosphate isomerase isozyme patterns, is usually complete (greater than 95%) in the peripheral blood, bone marrow, and hemopoietic stem cell compartments of long-term (greater than 3 months posttransplantation) AF chimeras. We report here, however, that splenic, lymph node, and thymic leukocytes of AF chimeras represent donor/host chimeric populations. Spleen cell populations of AF chimeras exhibit substantial chimera-to-chimera variation in the preponderant residual host cell type(s) present. Our interpretations of the implications of these findings are discussed.

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PubMed1985

Lung allograft rejection in the rat. I. Accelerated rejection caused by graft lymphocytes.

To find out to what extent rejection of lungs differs from that of other organs, functional rejection of lung allografts was studied in five combinations of inbred rat strains. Rejection could be monitored accurately by perfusion scintigraphy, and equally well by chest roentgenography. The rejection of lung grafts was found to proceed remarkably fast, when compared with heart grafts, in combinations with strong RT1-incompatibilities. This accelerated rejection pattern could be converted into rejection at a normal pace by pretreatment of the donor with 10 Gy roentgen irradiation one day before transplantation. Donor pretreatment depleted the lung graft's bronchus-associated lymphoid tissue (BALT) of lymphocytes. When grafts were depleted of all other passenger cells as well--by retransplantation from a cyclosporine-treated intermediate host--they showed an even more reduced immunogenicity, probably because of the loss of donor-type dendritic cells. These results indicate that lymphocytes from the BALT of lung grafts are capable of accelerating the rejection response.

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PubMed1985

Selective lymphoid irradiation. VI. Effect of palladium-109-labeled lymphocytes on rat cardiac allograft survival.

We have previously shown that pretransplant treatment with palladium-109 hematoporphyrin (Pd-H) and two small doses of antilymphocyte globulin (ALG) leads to donor-specific permanent acceptance of cardiac allografts in weakly histoincompatible rat combinations and significant prolongation of hearts in the ACI-to-Lewis strains. Pd-H also concentrates in nonlymphoid organs to a significant degree that is undesirable, so we have examined, in the present study, the efficacy of Pd-109 attached to lymphocytes in producing selective lymphoid irradiation and compared it with the immunosuppressive effect of Pd-H. Adoptive transfer of syngeneic lymphocytes labeled with palladium-109 (Pd-L) led to significant concentration of radioactivity in the peripheral lymphoid organs relative to the bone marrow (BM), intestine, thymus, and endocrine organs. The concentration of radioactivity in the spleen relative to BM and intestinal mucosa was 23:1 and 58:1, respectively. The immunosuppressive efficacy of a suboptimal dose of 3 mCi (one-third of the dose used in our earlier reports with Pd-H) administered via Pd-L (6 X 10(9) cells) at 4 days combined with 5 mg ALG at 2 days and 1 day prior to transplantation was compared in its effect on cardiac allografts with a similar dose of Pd-H (3 mCi) combined with ALG. The mean survival time (MST) of 6.5 +/- 0.4 days in untreated recipients was moderately prolonged to 14.6 +/- 3.0 days by Pd-H and ALG, and was not significantly different from an MST of 14.1 +/- 0.3 days achieved with 2 doses of ALG alone. Pretransplant treatment of Lewis rats with Pd-L and ALG produced a significant prolongation of ACI heart allografts to 30.5 +/- 3.1 days (P less than 0.001). These results suggest that Pd-L is more effective in prolonging rat cardiac allografts than a similar dose of Pd-H, and thus it may be a new method of selective lymphoid irradiation prior to transplantation.

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PubMed1986

The entry of lymphocytes into stimulated lymph nodes. The site of selection of alloantigen-specific cells.

During a primary response to antigen, lymph nodes (LN) receive antigen-specific lymphocytes (ASL) from the recirculatory pool via specialized postcapillary venules (SPCV). Preliminary experiments demonstrated a three-fold increase in entry of 51Cr-labeled thoracic duct lymphocytes (TDL) into the rat popliteal LN 3-4 days after alloantigenic stimulation. This increased entry was accounted for by an associated 4-5-fold increase in LN blood flow. It was unclear whether recruitment of ASL occurred within the SPCV lumen leading to selective entry of ASL--or, more conventionally, that entry of lymphocytes was a random process and that recruitment of ASL occurred in the extravascular space by selective retention. Thus a double-labeling technique was used to study the migratory characteristics of two populations of thoracic duct lymphocytes (TDL) that had been passaged from blood to lymph. The first population, passaged through a semiallogeneic animal, was negatively selected, and thus 99% depleted of ASL; the second population, passaged through a syngeneic animal, contained a normal complement of naive ASL. The two populations were combined before i.v. injection into syngeneic recipients. At 24 hr the right popliteal LN, which had previously been stimulated with the specific antigen, showed a preferential localization of the TDL containing ASL compared with the left (unstimulated) popliteal LN. This preferential localization was not present at 1 hr after injection. In the light of background data on the kinetics of lymphocyte traffic it is concluded that ASL were selected not at the luminal surface of SPCV but in the LN after they had left the bloodstream.

Animals↗
PubMed1986

Abrogation of the immunosuppressive effect of donor spleen cells on renal allografts in the rat by irradiation or heat treatment.

In the donor-recipient strain combination Lewis (RT1l) to Dark Agouti (RT1a), indefinite renal allograft survival (MST greater than 100 days) was induced by pretreating recipient animals i.v. with 10(6) to 10(8) viable spleen lymphocytes, seven days before transplantation. Pretreatment with 10(4) or 10(5) cells was ineffective (MST 10 days). However when 10(7) live, but heat-treated (55 degrees C for 10 min) or irradiated (1000 rads) cells were used, all the animals rejected the allograft in a normal fashion (MST 10 and 11 days, respectively). Median survival time of third-party controls was 10 days. The relative amount of cell surface major histocompatibility antigens (class I and class II) expressed by the three spleen cell preparations was investigated using monoclonal antibodies and fluorescence activated cell sorter analysis and found to be similar. After 24 hr in culture, only 1% of heat-treated and 10% of irradiated cells were viable, in contrast to 75% of untreated splenocytes. Trafficking of these lymphocytes in recipient animals was investigated by 51chromium labeling of the cells: 30% of lymphocytes had localized in the liver within 3 hr with little difference in localization among the different cell preparations. But, although 20% of normal and irradiated cells localized in the spleen within 3 hr, at no stage were more than 5% of the heat-treated cells found in the spleen. It is suggested that the length of time viable donor lymphocytes remain in the recipient circulation is important in the induction of specific immunosuppression by spleen lymphocytes.

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PubMed1988

Failure of freshly inplanted alloantigen in vivo to attract circulating allosensitized lymphocytes.

The important role served by donor-specific T lymphocytes in allograft rejection is well accepted. However, the mechanisms that attract the first alloreactive T cells to the graft are unclear. This study was performed to determine whether circulating specifically sensitized lymphocytes are attracted to alloantigen expressed on the surface of donor cells prior to the initiation of inflammatory reactions by the host. 111Indium-oxine labeled, bulk sensitized lymphocytes were injected intravenously into syngeneic mice bearing allogeneic and syngeneic peritoneal exudate cells in opposite hind footpads. Initially, twice as many sensitized lymphocytes were attracted to feet bearing the syngeneic peritoneal cells rather than the allogeneic peritoneal cells. In fact, the activity recovered from the allogeneic peritoneal cell depot was no greater than a contralateral footpad bearing media alone. This selective recruitment was present as early as 30 min following the transfer of radiolabeled cells. Furthermore, the labeled specifically sensitized lymphocytes were attracted to syngeneic macrophages within the peritoneal cell population. No other syngeneic and no allogeneic cells, at all, were capable of attracting circulating sensitized cells. Like specifically sensitized lymphocytes, thymocytes and concanavalin A blasts preferentially homed to sites of syngeneic macrophage deposition. Finally, clones of allospecific cytolytic and helper T cells also failed to migrate to sites of the specified donor alloantigen deposition. Thus, highly immune T cells accumulated, preferentially at sites of syngeneic macrophage inoculation. There is therefore no evidence to support the hypothesis that circulating specifically sensitized lymphocytes are attracted to alloantigen in vivo. Rather, it appears that the initial attraction of specifically sensitized, as well as unsensitized, lymphocytes is directed toward syngeneic macrophages. These data lend support to the hypothesis that the development of alloimmunity within the allograft may be initiated by host macrophages participating in normal healing responses.

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PubMed1988

Drug-induced in vitro tolerance to allogeneic antigens. II. Further analysis of in vitro-tolerized spleen cells in a fully allogeneic murine combination.

C3H/HeSlc (C3H, H-2k) spleen cells were made tolerant in vitro to C57BL/6CrSlc (B6, H-2b) at the cell-mediated cytotoxicity (CMC) level by in vitro stimulation for 48 hr with mitomycin C (MMC)-treated B6 spleen cells, and treatment with 5 micrograms/ml of 5-fluorouracil for a further 9 hr. These cells were given intraperitoneally to neonate (C3HxB6) F1 mice to examine whether these tolerized spleen cells would cause lethal graft-versus-host disease (GVHD). Despite the lack of CMC, the tolerized C3H spleen cells caused lethal GVHD in most of the neonate F1 mice. Evaluating from various immune parameters, it was evident that T cell populations responsible for IL-2 production, cytostasis, and delayed footpad reaction (DFR) were retained intact after in vitro tolerance induction, probably because of their less-proliferative characteristics in response to fully allogeneic antigen stimulation, and were considered to be responsible for lethal GVHD. Contribution of natural killer (NK) cells to lethal GVHD was not ruled out.

Animals↗
PubMed1988

Major histocompatibility complex control of NK-related allogeneic lymphocyte cytotoxicity in rats. The contributions of strong and medial transplantation antigens.

Allogeneic lymphocyte cytotoxicity (ALC) describes the elimination of allogeneic lymphocytes in vivo by an NK-related activity. There is evidence that ALC is demonstrable between donor and recipient when these are incompatible at MHC gene loci alone. Since ALC is a property of T cell-deficient nude rats, the role of the MHC in this rejection process needs further study. We have determined the contribution of the MHC to ALC using congenic and recombinant rats. In our analysis we have assumed that ALC involves the recognition of classic alloantigens by clonally distributed effector cells as for other examples of transplant rejection, although this is not yet proved. Strong ALC was measured between congenic rats that differed for MHC genes only. Non-MHC incompatibility alone did not elicit ALC. In the presence of MHC incompatibility the strength of ALC generated in a recipient was dependent on non-MHC genes. The PVG background generated high ALC responses whereas ALC was not measured in the DA rat. However ALC was measured in the congenic PVG-RT1avl (DA) rat. The contributions of classic class I (RT1.A), class II (RT1.B/D), and medial transplantation (RT1.C) regions of the rat MHC were determined by comparing different recombinant donors into the same recipient strain. Single region differences alone in any of these three MHC regions did not elicit full ALC. In two sets of transfers a combination of RT1.B/D and RT1.C region incompatibility was sufficient to generate a full allogeneic response. It can be concluded that the controlling element for allogeneic lymphocyte cytotoxicity is in the RT1.B/D-RT1.C region of the rat MHC.

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PubMed1990

The effects of perioperative portal venous inoculation with donor lymphocytes on renal allograft survival in the rat. I. Specific prolongation of donor grafts and suppressor factor in the serum.

In order to investigate the in vivo functional role of the liver in the immune responses in organ transplantation, effects of perioperative portal venous p.v. administration of donor lymphocytes on renal allograft survival were tested in the rat kidney transplant model. Donor lymphocytes were prepared from BN (BN, RT-1n) or third-party DA (RT1a) rat spleens and lymph nodes and injected p.v. or intravenously to Lewis (LEW, RT-1l) hosts on the day of transplantation (day 0). Untreated LEW hosts rejected BN renal grafts at 7.8 +/- 0.6 days (n = 10). Intravenous administration of 1 x 10(8) BN cells to LEW hosts on day 0 caused a slight, but not significant, prolongation of renal allograft survival (MST = 9.5 +/- 3.0 days, n = 13, NS), whereas portal venous inoculation of 1 x 10(8) BN cells on day 0 remarkably prolonged renal graft survival to 22.2 +/- 5.3 (n = 10, P less than 0.01). The prolongation of graft survival was antigen-specific; the administration of 1 x 10(8) DA cells p.v. to LEW hosts did not prolong the survival of BN renal grafts (MST = 7.4 +/- 0.8, n = 5). Spleen cells from p.v. treated LEW hosts 10 days after transplantation had no suppressor effect on the one-way MLC reaction of normal LEW responder cells toward donor BN or third-party DA stimulators. On the other hand, when serum from p.v.-treated LEW hosts was added to MLC at a concentration of 3 per cent of total volume, it suppressed the MLC reaction toward donor BN cells by 71.6 per cent, but not toward third-party DA stimulators (-8.5 per cent suppression, NS). Histological examination of p.v.-treated LEW hosts at 10 days after transplantation revealed that the liver had normal lobular architecture without expansion of portal tracts and infiltration of inflammatory cells. On the other hand, the transplanted kidney demonstrated a moderate mononuclear cell infiltration around the artery without an interstitial hemorrhage. Moreover, adoptive transfer of the serum from p.v.-treated LEW rats into the virgin secondary LEW hosts significantly prolonged the graft survival of BN kidneys from 7.8 days to 18.9 +/- 5.5 days (P less than 0.01), but not third-party DA graft survivals (MST = 7.5 +/- 0.6 days), indicating that an antigen-specific tolerogenic factor was released into the circulation through the process of allogeneic cells in the liver.

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