Gender and physical therapy career success factors.

BACKGROUND AND PURPOSE: Gender and profession are thought to affect how career success is perceived as well as how it is achieved. This study investigated items considered important in defining career success for male and female physical therapists. The study also explored the relationship among gender, beliefs about career success, and career experiences. SUBJECTS AND METHODS: Data were obtained through an investigator-developed survey. The self-report questionnaire consisted of 78 items in 4 areas: descriptive information, items important in characterizing career success, items perceived to enhance or inhibit career success, and items assessing self-esteem. Questionnaires were mailed to a random sample of active physical therapist members of the American Physical Therapy Association (N = 5,000). The response rate was 38.1% (n = 1,906). RESULTS: Both men and women selected indicators such as practicing ethically, improving patient health, and feeling satisfied over high income or status when describing career success. All respondents agreed that clinical competency and motivation are key factors related to achieving career success. Family issues, full-time employment, and flexibility of practice conditions emerged as primary gender differences. CONCLUSION AND DISCUSSION: A unique set of indicators describe physical therapy career success. Gender differences in its description and factors that influence its achievement are related primarily to family issues. Career success for women depends to a greater degree on the ability to manage family responsibilities in conjunction with employment opportunities.

Gender-based income differences for physical therapist managers.

BACKGROUND AND PURPOSE: The purpose of this study was to determine whether income differences associated with gender exist for therapists in management positions and whether such differences also exist for salaried and self-employed individuals after adjusting for differences due to hours worked, years worked full-time, leave taken from the profession, number of years at a facility, and number of years in a position. SUBJECTS: The subjects were 969 physical therapists who held management positions throughout the United States. METHODS: Subjects responded to a survey designed for male and female administrators. Respondents were assigned to groups of salaried therapists or self-employed therapists, t tests were used to compare characteristics based on gender, and analysis of covariance was used to compare income based on gender after controlling for certain variables. RESULTS: After adjusting for the set of five covariates, the data showed that self-employed female therapists earned 77% of the average salary earned by the self-employed male therapists. A similar analysis revealed that the salaried female managers earned 89% of the average salary earned by male managers. Within the five practice subgroups of salaried managers, salary differences existed only for those therapists working in acute care settings. CONCLUSION AND DISCUSSION: For the physical therapist managers who responded to the survey, there were gender-based salary differences. Regardless of whether the therapists were salaried or self-employed, salary differences existed for some areas of practice but did not appear to exist in other areas of practice.

Activation of virus replication after vaccination of HIV-1-infected individuals.

Little is known about the factors that govern the level of HIV-1 replication in infected individuals. Recent studies (using potent antiviral drugs) of the kinetics of HIV-1 replication in vivo have demonstrated that steady-state levels of viremia are sustained by continuous rounds of de novo infection and the associated rapid turnover of CD4+ T lymphocytes. However, no information is available concerning the biologic variables that determine the size of the pool of T cells that are susceptible to virus infection or the amount of virus produced from infected cells. Furthermore, it is not known whether all CD4+ T lymphocytes are equally susceptible to HIV-1 infection at a given time or whether the infection is focused on cells of a particular state of activation or antigenic specificity. Although HIV-1 replication in culture is known to be greatly facilitated by T cell activation, the ability of specific antigenic stimulation to augment HIV-1 replication in vivo has not been studied. We sought to determine whether vaccination of HIV-1-infected adults leads to activation of virus replication and the targeting of vaccine antigen-responsive T cells for virus infection and destruction. Should T cell activation resulting from exposure to environmental antigens prove to be an important determinant of the steady-state levels of HIV-1 replication in vivo and lead to the preferential loss of specific populations of CD4+ T lymphocytes, it would have significant implications for our understanding of and therapeutic strategies for HIV-1 disease. To begin to address these issues, HIV-1-infected individuals and uninfected controls were studied by measurement of immune responses to influenza antigens and quantitation of virion-associated plasma HIV-1 RNA levels at baseline and at intervals after immunization with the trivalent influenza vaccine. Influenza vaccination resulted in readily demonstrable but transient increases in plasma HIV-1 RNA levels, indicative of activation of viral replication, in HIV-1-infected individuals with preserved ability to immunologically respond to vaccine antigens. Activation of HIV-1 replication by vaccination was more often seen and of greater magnitude in individuals who displayed a T cell proliferative response to vaccine antigens at baseline and in those who mounted a significant serologic response after vaccination. The fold increase in viremia, as well as the rates of increase of HIV-1 in plasma after vaccination and rates of viral decline after peak viremia, were higher in individuals with higher CD4+ T cell counts.(ABSTRACT TRUNCATED AT 400 WORDS)

IL-10 inhibits IL-7-mediated murine pre-B cell growth in vitro.

B lymphopoiesis in the bone marrow is mediated by both positive and negative regulatory cytokines. In this report, we demonstrate that interleukin-10 (IL-10) may function to inhibit murine IL-7-dependent pre-B cell growth. Recombinant IL-10 (rmIL-10) inhibited BALB/c bone marrow IL-7 colony-forming unit (CFU) in a concentration-dependent manner, and growth was restored when IL-10 was neutralized with the monoclonal anti-IL-10 antibody, SXC-1. Enriched populations of B220+ bone marrow B lineage cells were also inhibited in their responses to IL-7 by exposure to rmIL-10, suggesting that pre-B cells were directly susceptible to rmIL-10 inhibition. Heterogeneity in the capacity of IL-7 CFU to be inhibited by IL-10 was evident. Although 60% of IL-7 CFU were inhibited by rmIL-10 at 5 U/mL, approximately 20% of IL-7 CFU were not inhibited by rmIL-10 concentrations up to 50 U/mL. Prior incubation of bone marrow cells for 24 hours with IL-7 prevented rmIL-10-mediated growth inhibition, suggesting that prior rIL-7 stimulation of pre-B cells abrogates the inhibitory effects of rmIL-10. These experiments indicate that IL-10, at these concentrations, may function as a potent negative growth regulator for a significant fraction of IL-7-responsive pre-B cells.

IL-7 drives donor T cell proliferation and can costimulate cytokine secretion after MHC-matched allogeneic bone marrow transplantation.

Transplantation of MHC-matched, allogeneic B10.D2 bone marrow plus T cells into BALB/c recipients ultimately results in chronic graft-vs-host disease (GVHD) and mortality 8 to 12 wk post-transplant. We have identified IL-7-specific mRNA in the spleens of BALB/c bone marrow transplantation (BMT) recipients during the first week post-transplant. The response by T cells from B10.D2-->BALB/c BMT recipients to stimulation with IL-7 in vitro during the early period after transplant was then examined. The findings indicated that within the first week post-transplant, spleen cells removed from recipients injected with allogeneic, but not syngeneic, T cells proliferated vigorously to rIL-7. Both IL-2-dependent and -independent components were identified. Depletion of responding cells before culture with anti-Thy-1.2 Ab virtually eliminated this response. We conclude that transplant of allogeneic T cells is required for the observed IL-7 response, and moreover, such cells proliferate after exposure to this cytokine in vitro. To determine whether IL-7 could have a functional effect on donor T cells, the production of IFN-gamma by T cells from allogeneic BMT recipients stimulated with anti-T cell receptor (i.e., anti-V beta) Ab was examined. IL-7 was demonstrated to enhance IFN-gamma production by donor T cells postallogeneic BMT. These results suggest that a cytokine presumably produced in the host for the physiologic function of hematologic reconstitution is playing an additional role during the early events after allogeneic BMT mediated via the expansion and augmented cytokine production by donor T cells.

Endogenous superantigens in allogeneic bone marrow transplant recipients rapidly and selectively expand donor T cells which can produce IFN-gamma.

Despite the existence of many non-MHC disparities between MHC matched but non-MHC mismatched donors and recipients, graft-versus-host disease (GVHD) is not clinically apparent following a significant number of allogeneic bone marrow transplants (BMT) in experimental animals. The present studies examined V beta TcR expression and IFN-gamma production by donor T cells in a BMT model involving an MHC matched, allogeneic donor-recipient combination which included a unidirectional superantigen disparity (Mls). B10.D2-->BALB/c, but not BALB/c-->B10.D2 recipients develop GVHD and mortality ensues 8-12 weeks post-transplant. During the first 2 weeks post-transplant of B10.D2-->BALB/c, approximately 50% of all Thy1.2+ spleen and lymph node cells were found to express T cell receptors utilizing V beta 3. A similar rapid and selective expansion of V beta 3+ TcR bearing donor T cells was detected in two other H-2 matched superantigen disparate donor-recipient BMT combinations. An increased percentage of V beta 3+ T cells was noted among both the CD4+ and CD8+ populations. Thus, in these donor/recipient combinations, all TcR families were not equally expanded early following transplant. At 4-10 days post-transplant, IFN-gamma specific mRNA was readily detected in the spleens of B10.D2-->BALB/cBMT recipients containing large numbers of V beta 3+ T cells. Moreover, V beta 3+ donor T cells from these recipients contained IFN-gamma mRNA. Specific stimulation in vitro with immobilized anti-TcR moAbs demonstrated that V beta 3+ T cells secreted a large amount of the total IFN-gamma levels detected. The ability of endogenous superantigens to activate large numbers of T cells which can produce cytokines after BMT indicates that when present, such antigenic differences may contribute to events occurring during initial graft-versus-host reactions. Such antigens could therefore participate in the events influencing whether GVHD develops following BMT between certain donors and recipients.

Suppression of B-cell development as a result of selective expansion of donor T cells during the minor H antigen graft-versus-host reaction.

A murine model of bone marrow (BM) transplantation in which donor (B10.D2) and recipient (BALB/c) mice were major histocompatibility complex (MHC) (H-2d) and Mls-1 identical, but incompatible at multiple non-MHC minor histocompatibility (H) antigens, and at Mls-2,3 was used to examine regeneration of B-cell development during the minor H antigen graft-versus-host reaction (GVHR). Mice that received T-cell-depleted allogeneic BM regained significant pre-B cells (sIg- 14.8+) in their BM. Mice undergoing GVHR after transplantation with allogeneic BM + T cells had less than 2% pre-B cells in their BM at day 7 and only 12% to 14% pre-B cells at days 21 and 28 compared with greater than 20% pre-B cells in the allogeneic controls. After partial recovery, the pre-B cells in the BM of GVH mice again decreased to less than 3% by day 42. This abnormal pattern of pre-B cell development in mice undergoing GVHR was associated with a reduced response to interleukin-7 (IL-7) in vitro. The delay in B-lineage cell reconstitution in mice with GVHR correlated with the expansion of donor V beta 3+ T cells in both the spleen and BM. BM T cells from mice with GVHR as well as isolated V beta 3+ T cells inhibited IL-7 colony-forming units from normal BM in co-culture assays. This inhibition could be reversed with anti-interferon gamma (IFN gamma) antibody. These data suggest that the delay in appearance and the reduction in proportion and number of pre-B cells observed early during the GVH reaction in this model is caused, in part, by the inhibitory actions of IFN gamma derived from donor V beta 3+ T cells on B-lineage cell development.

Antibody responses to bacteriophage phi X174 in patients with adenosine deaminase deficiency.

Adenosine deaminase (ADA) deficiency and its biochemical consequences cause severe combined immunodeficiency (SCID). Treatment strategies, designed to correct the biochemical abnormalities, include transplantation of matched bone marrow or haploidentical bone marrow stem cells, repeated partial exchange transfusions with frozen irradiated human red blood cells (RBC), or weekly injection of polyethylene glycol-modified bovine ADA (PEG-ADA). To evaluate the effect of these therapeutic options, we studied in vitro T-cell function and in vivo antibody responses to the T-cell-dependent neoantigen, bacteriophage phi X174, in 10 children with ADA-deficient SCID. In untreated patients, T-cell function was severely depressed, and only minute amounts of antibacteriophage antibody were produced. Transplantation of bone marrow from a matched sibling (one patient) or a phenotypically matched parent (one patient) resulted in a stable graft, normal T-cell function, and substantial but subnormal antibody titers to bacteriophage, with reduced memory and impaired switch from IgM to IgG. Patients receiving T-cell-depleted haploidentical bone marrow stem cells had markedly depressed antibody responses for as long as 3 years posttransplantation, despite rapidly improving T-cell function that became normal in two of four patients. Two methods of enzyme replacement were explored. During treatment with human RBC transfusions, antibody responses to bacteriophage were as severely depressed as in untreated ADA-deficient patients. Treatment with weekly injections of PEG-ADA resulted in normalization of T-cell numbers in all four patients, normal or near-normal T-cell function in two, and mildly but variably improved T-cell function in the other two patients. Quantitatively and qualitatively normal antibody responses to bacteriophage were observed in three of four patients. Assessment of antibody responses to immunization with bacteriophage phi X174 is a useful method to monitor humoral immune function in treated ADA-deficient patients and can be used to estimate when intravenous immunoglobulin (IVIG) prophylaxis may be safely discontinued.

Why students choose occupational therapy as a career.

To recruit students to occupational therapy, we need to know what prospective students seek in careers. A survey consisting of an attitude inventory was sent to 403 current occupational therapy students with a response rate of 54%. Earlier research identified that students had primarily altruistic goals in selecting occupational therapy as a profession, and this study continued to find that students wanted to help others; however, this was not a predictor of their favoring the profession. A factor analysis of the inventory revealed that students chose occupational therapy as a career because they liked the salaries, nationwide job availability, regular hours, and prestige that is associated with the profession. Students were more positive about the profession if they had experience working in occupational therapy departments, and 40% reported that no specific persons had influenced their career decision.

The role of hematogenous and intrinsic precursor cells in lymphocyte production in murine bone marrow and thymus.

It is well recognized that the bone marrow contains cells that can repopulate a depleted thymus as well as cells that can be induced to express phenotypic markers characteristic of T cells. It is not known, however, to what extent thymocytopoiesis in the normal thymus relies on immigrant, bone marrow-derived cells, nor whether some T cell precursors have entered the bone marrow from the circulation. We used the parabiotic system to test whether thymocytopoiesis relies on progenitors intrinsic to the thymus or on cells that enter the organ from the circulation. In the same system, we have also investigated whether Thy-1- bone marrow lymphocytes that respond to phytohemagglutinin (PHA) by proliferation and Thy-1 expression are produced by myelogenous or hematogenous progenitors. Syngeneic CBA/HT6 and CBA/CaJ mice were joined in parabiotic union at 4-6 weeks of age. Cross circulation between the two partners was verified by the equilibration of Evans' blue dye injected into one partner and by the equilibration of PHA-responsive T cells in the spleen of the parabionts. Chromosome spreads were prepared from the PHA-stimulated T cell-depleted bone marrow and from spontaneously proliferating thymocytes as well as from thymocytes stimulated by PHA or Concanavalin A (Con A). The exchange of spleen colony-forming units (CFU-S) in the femoral marrow was assessed by karyotyping individual spleen colonies. Regardless of the length of parabiotic union, ranging from 4 to 20 weeks, Thy-1-, PHA-responsive bond marrow lymphocytes remained predominantly of the host type with only 3% being derived from the opposite partner.(ABSTRACT TRUNCATED AT 250 WORDS)

The murine forestomach: a sensitive site for graft-versus-host disease.

The minor histoincompatible mouse radiation chimera provides a useful model of graft-versus-host disease (GVHD) paralleling conditions in human marrow transplant recipients. While studying the B10.D2/BALB/c model, we noted that a graft-versus-host reaction of particular severity develops in the forestomach near the squamocolumnar junction. Comparison of the dyskeratotic index of this epithelium with that of the skin of the same animal revealed the forestomach to be a more sensitive site for detection of GVHD. In normal mice, both basal forestomach squamous epithelium and cells in the lamina propria expressed class II antigens. During the course of GVHD, class II antigen expression was elevated in the squamous epithelium of the forestomach, the columnar epithelium associated with the stomach, and cells within the associated lamina propria. The demonstration here that the squamocolumnar junction (considered to be a stem cell region for the maintenance of adjacent forestomach squamous epithelium) appears to be a particularly sensitive target tissue in GVHD and earlier identification of other epithelial target tissues of GVHD (hair follicles and rete ridges of epidermis, bile ductules of liver, and crypt cells of the gut) collectively support the hypothesis that GVHD tends to target sites of epithelial proliferation overlying epithelial stem cells.

Job satisfaction of occupational therapy faculty.

What causes occupational therapy faculty to be satisfied with their teaching roles? A survey of 538 occupational therapy faculty was conducted with questions that identified demographic information and inquired about specific satisfying and dissatisfying items. Responses indicated no strong correlations between demographic information and satisfaction items but did offer some implications that warrant attention. The faculty were satisfied with teaching in general and specifically with the academic environment, the opportunity to design learning experiences, and the lack of constraints in higher education. The results of this study may help educational administrators make decisions that will foster recruitment, retention, and socialization of occupational therapy faculty.

Immune dysfunction associated with graft-versus-host reaction in mice transplanted across minor histocompatibility barriers. I. Depressed antigen-specific antibody responses to bacteriophage phi chi 174.

The effect of the graft-versus-host reaction in response to minor histocompatibility antigens on the antibody response to a T-dependent antigen was studied in four strains of mice. Lethally irradiated mice were transplanted with bone marrow plus graded numbers of spleen cells from H-2-compatible donors. Recipients of syngeneic bone marrow transplants and recipients of allogeneic bone marrow depleted of T cells made normal antibody responses to bacteriophage phi chi 174 when immunized on day 28 (primary) and day 56 (secondary) after marrow transplantation. Recipients of allogeneic bone marrow plus spleen cells made only small amounts of specific antibody and failed to make IgG antibody after secondary immunization. The pattern of the depressed antibody response suggests that the primary mechanism of immune dysfunction in mice with the minor antigen GVHR is a lack of T helper cell function.

Immune dysfunction associated with graft-vs-host reaction in mice transplanted across minor histocompatibility barriers. II. Reversible defect in T-dependent antibody responses.

B cell and Th cell functions were assessed in mice undergoing a graft-vs-host reaction (GvHR) in response to minor histocompatibility Ag by using the plaque-forming cell (PFC) response to the T-independent Ag TNP-Brucella abortus and the T-dependent Ag TNP-SRBC. Bone marrow plus spleen cells from B10.D2 mice were transplanted into lethally irradiated B10.D2 (syngeneic recipient) or H-2d-compatible BALB/c (allogeneic recipient) to produce a chronic form of GvHR. BALB/c recipients of an allogeneic transplant demonstrated a marked and proportional lymphoid depletion of the spleen with normal percentages of B cells, T cells, and CD4+ and CD8+ T cell subsets. Mice with GvHR made normal numbers of PFC/10(5) spleen cells in response to the T-independent Ag, but a significantly depressed number of PFC/10(5) spleen cells to the T-dependent Ag compared with normal B10.D2 mice and with irradiated B10.D2 recipients of syngeneic B10.D2 marrow plus spleen cells. Mice undergoing the minor Ag GvHR made significantly larger numbers of PFC/10(5) spleen cells after secondary immunization with TNP-SRBC compared with controls. In vitro assays demonstrated that B cells from mice with GvHR responded to T help from normal B10.D2 mice and that T cells from mice with GvHR provided help to normal B cells after in vivo immunization. These data demonstrate that radiation chimeras with GvHR in response to minor histocompatibility Ag have relatively normal B cell function and an apparent defect in T helper cell function that is reversible by immunization with appropriate Ag.

Mechanism of immune dysfunction associated with minor antigen graft-vs-host disease in mice.

A well-characterized murine model of graft-vs-host disease (GVHD) that develops in response to minor histocompatibility antigens was used to study the mechanism of an immunodeficiency syndrome that is associated with GVHD. Lethally irradiated mice were transplanted with a combination of bone marrow and spleen cells from H-2 compatible donors that differed at multiple minor histocompatibility antigens, or from syngeneic donors. Four to 12 weeks later, the humoral responses of transplanted and control mice to the T dependent antigens bacteriophage phiX174 and TNP-sheep red blood cells (TNP-SRBC), and to the T independent antigen TNP-Brucella abortus (TNP-BA) were determined. The results demonstrate that mice with GVHD have relatively intact B Cell function and a profound defect in T helper cell function. The immune response to T dependent antigens normalized with repeated immunization. We conclude that immune dysfunction in mice with GVHD is due to a reversible defect in T helper cell function.

Maternally induced graft-vs-host disease to minor antigens as a possible etiology of an acquired immunodeficiency syndrome in mice.

It has been postulated that an acquired immunodeficiency syndrome develops in neonates as the result of a maternally induced graft-vs-host disease (GVHD) that develops when sufficient numbers of maternal lymphocytes are transferred to the fetus across the placental barrier. The present study was done to determine whether major histocompatibility complex (MHC) antigens or non-MHC minor histocompatibility antigens (MiHA) were involved. Female C57BL/6 mice were bred to males of eight selected strains such that maternal-fetal disparity existed at MHC antigens and/or minor histocompatibility antigens. Offspring were tested for immune function at 6-7 weeks of age using a Jerne plaque assay to measure the humoral response to that T dependent antigen sheep red blood cells (SRBC). None of the offspring developed clinical signs of GVHD, but 3 of 124 mice tested made no immune response to SRBC. Immunodeficiency was associated with maternal-fetal disparity only at a small number of MiHA and not at the MHC. We postulate that immunodeficiency in this model is mediated by a subclinical maternally induced GVHD to paternally derived MiHA of the fetus.

Effect of maternal-fetal histoincompatibility on the weight of the feto-placental unit in mice: the role of minor histocompatibility antigens.

Female mice from four congenic strains were bred to males of the same four strains to determine the effect of maternal-fetal disparity at major histocompatibility complex (MHC) and the effect of non-MHC minor histocompatibility antigens on the weight of the feto-placental unit. An increase in feto-placental weights was found in all three of the four strains that could be evaluated when mother and fetus differed at multiple minor histocompatibility loci, irrespective of whether disparity at the MHC was present. No increase in feto-placental weights was found when mother and fetus differed at the MHC alone. The fact that these results were found in all strains studied suggests that the effect of maternal-fetal disparity at multiple minor histocompatibility antigens (minor HA) on the weight of the feto-placental unit is biologically significant. We conclude that if the increase in weight of the feto-placental unit results from immunostimulation, then minor histocompatibility antigens are the primary target of the maternal immune response to the histocompatibility antigens of the fetus.

Inhibitory control of proximal colonic motility by the sympathetic nervous system.

The purpose of this study is to determine whether or not the sympathetic nervous system provides a tonic inhibitory input to the colon in chloralose-anesthetized cats. Proximal and midcolonic motility were monitored using extraluminal force transducers. An intravenous bolus injection of 5 mg of phentolamine in 14 animals elicited a pronounced increase in proximal colon contractility. The minute motility index changed from 0 +/- 0 to 26 +/- 4 after phentolamine administration. Midcolonic motility also increased in response to phentolamine. Specific blockade of alpha 2-receptors, but not alpha 1-receptors, caused the same response seen with phentolamine. alpha-Adrenergic blockade increased colon contractility after spinal cord transection but not after ganglionic blockade. Blockade of alpha-adrenergic receptors was also performed before vagal and pelvic nerve stimulation and in both cases increased colonic motility. Vagal stimulation alone had no effect on colonic contractility, while pelvic nerve stimulation increased motility at the midcolon. alpha-Receptor blockade did not alter the ineffectiveness of vagal stimulation but did unmask excitatory effects of pelvic nerve stimulation on the proximal colon. All excitatory colonic responses were prevented by blocking muscarinic cholinergic receptors. These data indicate that tonic sympathetic nervous system activity exerts an inhibitory effect on colonic motility. The inhibitory effect is mediated through alpha 2-adrenergic receptors. Based on these findings, we suggest that alterations in sympathetic nervous system activity may be extremely important for the regulation of circular muscle contractions in the colon.

L3T4-positive T cells participate in the induction of graft-vs-host disease in response to minor histocompatibility antigens.

The phenotype of T cells that initiate graft-vs-host disease (GVHD) in response to minor histocompatibility antigens (minor HA) was determined in three H-2 compatible strain combinations by using negative selection with monoclonal antibodies to Lyt-2 and L3T4 antigens to test the hypothesis that Lyt-2-positive T cells alone initiate GVHD. The phenotype of T cells required to initiate GVHD was different in each of the three strain combinations studied. Both Lyt-2+ and L3T4+ LP spleen cells were necessary to cause lethal GVHD in C57BL/6 recipients. In the reciprocal transplant, Lyt-2+, but not L3T4+ C57BL/6 spleen cells were sufficient to initiate GVHD in LP recipients. In contrast, L3T4+, but not Lyt-2+ B10.D2 spleen cells were found to initiate GVHD in BALB/c recipients. The optimal response to minor HA requires both Lyt-2+ and L3T4+ T cells because a mixture of the two subsets of spleen cells resulted in a more severe form of GVHD than either subset alone in all three strain combinations studied. This study demonstrates that L3T4+ cells participate in the initiation of GVHD in response to minor HA. The dominant T cell subset that initiates GVHD varies with the specific strain combination tested. The specific minor HA expressed in the transplant recipient, the H-2 type, and possibly non-major histocompatibility complex immune response genes of the donor strain appear to determine the phenotype of the initiator T cells.

Environmental influences on immunologically associated spontaneous abortion in CBA/J mice.

CBA/J female mice mated to DBA/2 male mice have a high level of fetal resorption. The rate of resorption can be influenced by the environment in which the animals are maintained.