Cross reactions in the H-2 system of cytotoxic T-lymphocytes concentrated by the adsorption-elution method on target cell monolayers]

Cytotoxic T-lymphocytes (CTL) obtained by in vivo immunization were enriched by the absorption-elution technique, using the relevant allogeneic target cell (TC) monolayers. After the separation of C57BL anti-A (anti-KkDd) lymphocytes into anti-Kk and anti-Dd subpopulations they displayed cross killing cytotoxic effect on H-2d and H-2kTC, respectively. B10D2 anti-B10 (anti-KbDd) lymphocytes cross reacted to H-2a and H-2q TC. The results are discussed in the light of heterogeneity of CTL clones or their receptors.     

Immunity to leprosy. II. Genetic control of murine T cell proliferative responses to Mycobacterium leprae

T cell proliferative responses to Mycobacterium leprae were measured after immunization of mice at the base of the tail with antigen and challenging lymphocytes from draining lymph nodes in culture with M. leprae. This T cell response to M. leprae has been compared in 18 inbred strains of mice. C57BL/10J mice were identified as low responder mice. The congenic strains B10.M and B10.Q were found to be high responders, whereas B10.BR and B10.P were low responders. F1 (B10.M X C57BL/10J) and F1 (B10.Q X C57BL/10J) hybrid mice were found to be low responders, similar to the C57BL/10J parent, indicating that the low responsive trait is dominant. Whereas B10.BR mice were shown to be low responders to M. leprae, B10.AKM and B10.A(2R) were clearly high responders, indicating that the H-2D region influences the magnitude of the T cell proliferative response. Gene complementation within the H-2 region was evident. Genes outside the H-2 region were also shown to influence the response to M. leprae. C3H/HeN were shown to be high responder mice, whereas other H-2k strains, BALB.K, CBA/N, and B10.BR, were low responders. Gene loci that influence the T cell proliferation assay have been discussed and were compared to known background genes which may be important for the growth of intracellular parasites. Because mycobacteria are intracellular parasites for antigen-presenting cells, genes that affect bacterial growth in these cells will also influence subsequent immune responses of the host.     

A study of H-2 mutations in mice. V. Detection of mutations M505, Hzl and M506 in the host vs transplant reaction]

H-2 mutant/normal pairs of congenic mouse strains C57BL/6equilibriumB6.M505 (H-2Kbd), C57BL/6equilibriumB6.C(Hz1) (H-2Kba) and A.CAequilibriumA.CA(M506) (H-2fa) were studied in the graft versus host assay. All the three mutations were expressed in these tests as gain and loss of H-2 antigen. The data obtained confirm an earlier suggestion that the H-2K antigenic molecule bears antigenic determinants which could be detected by a variety of immunological techniques.     

Allogeneic lymphocyte induction in vivo of highly active T-killers specific for the molecule of the H-2 class-I complex and the detection of their receptors in vitro

The optimal conditions are found for in vivo irradiated lymphocyte induction of high cytotoxic T lymphocytes (CTL) specific to the H-2Kb molecule with a subsequent monoculture differentiation. B10.D2(R101) CTL have a pronounced excess as compared to B10.A (4R) CTL, with respect to lysis intensity of the same target cells (TC), and requires a lower term of the monoculture incubation in spite of their specificity to the same H-2Kb molecule. As the susceptibility of TC for CTL lysis is higher (M phi as compared to EL-4 thymoma cells), CTL are much more inactivated with the monoclonal antibodies to Lyt-2 and Lyt-3 antigens without complement. Anti-H-2Kb CTL differentiated in the monoculture cross react to TC bearing third-party H-2 molecules (Kk, Dq, Dk). Unlike a stable CTL adherence to the donor M phi monolayer, nonspecific CTL adherence to the syngeneic M phi monolayer declines in the presence of EGTA, and as a result of repeated detachment of lymphocytes. The findings give rise to study receptor affinity expressed on the in vivo induced CTL surface, the CTL receptor monoclonal antibody and the CTL differentiation factor.     

Estimates of the precursor frequency of cytotoxic T lymhocytes against antigens controlled by defined regions of the H-2 gene complex: comparison of the effect of H-2 differences due to intra-H-2 recombination vs mutation.

Lymph node cells were sensitized in a limiting dilution assay against B10.D2 (H-2d) and the frequency of cytotoxic T lymphocyte (CTL.P) precursors was determined. A mean CTL.P frequency of 0.047% was observed when responding strains differed from the stimulators at the entire H-2 gene complex. When intra-H-2 recombinant strains were sensitized against B10.D2, lower frequencies of CTL.P were observed. Responding strains that differed from the stimulators at the H-2K-end only had 2- to 6-fold more CTL.P compared to strains sensitized against the D-end only. In order to study the CTL.P frequency against minor antigenic differences, the B10.D2 (M504-H-2da) mutant strain, which carries a mutation with an antigenic gain-loss in the D-region of H-2d, was examined. This mutant showed an identical CTL.P frequency against H-2d as H-2D-end recombinant strains. Therefore, this H-2 mutant (M504) has either undergone extensive mutation or the qualitative nature of the antigenic loss in this strain results in a high CTL.P frequency against the strain of origin.     

IgE formation and Fc receptor-positive lymphocytes in normal, immuno-deficient, and auto-immune mice infected with Nippostrongylus brasiliensis

The IgE serum levels and IgE FcR-positive lymphocytes (Fc epsilon R) in the spleen and mesenteric lymph nodes (MLN) of normal and immunologically mutant strains of mice were determined before and 14 days after infection with Nippostrongylus brasiliensis (Nbr) parasites. By IgE rosetting of cells immunofluorescently stained for sIg. Thy-1.2, Lyt-2, and L3T4, only sIg+ IgE rosetting lymphocytes were detected in both normal and Nbr-infected mice. IgE high responder mice had the same percentage of Fc epsilon R+ spleen and MLN lymphocytes as low responder mice. After Nbr infection, the percentages of splenic and MLN Fc epsilon R+ cells increased in parallel to a similar increase of sIg+ B cells. Athymic C57BL/6J-nu mice had 62% Fc epsilon R+ spleen and 85% Fc epsilon R+ MLN cells before and after Nbr infection, but IgE serum levels were less than 5 ng IgE/ml. C57BL/6J mice with the viable moth-eaten mutation mev which have almost exclusively Ly-1+ B cells, had less than 1% Fc epsilon R+ lymphocytes and formed only small amounts of IgE. C57BL/6J mice with the lymphoproliferation (lpr) or generalized lymphoproliferative disease (gld) mutations had low numbers of Fc epsilon R+ cells but formed 15 to 30 times more IgE after Nbr infection than control C57BL/6J mice. The IgE response of mice with the beige mutation (bg) did not differ from control mice. Mice with the xid mutation had few Fc epsilon R+ and sIg+ cells but showed high IgE responses. These data demonstrate that Fc epsilon R are typical cell surface markers for approximately 90% of murine Ly-1-, sIg+ B cells and that the number of Fc epsilon R+ cells does not correlate with the capacity of the mice to form IgE. The IgE response to Nbr infection is normal in mice homozygous for the bg mutation, elevated in mice homozygous for the xid, lpr, and gld mutations, and decreased in mice homozygous for the mev and nu mutations.     

Lack of correlation of central nervous system inflammation and neuropathology with the development of seizures following acute virus infection

Infection of C57BL/6 mice by the intracerebral route with the Daniels (DA) strain of Theiler's murine encephalomyelitis virus (TMEV) resulted in acute behavioral seizures in approximately 50% of the mice. By titration, the viral dose correlated with the percentage of mice developing seizures; however, neuropathological changes were similar over the dose range, and viral clearance from the brains occurred uniformly by day 14 postinfection (p.i.). Other TMEV strains and mutants (GDVII, WW, BeAn 8386 [BeAn], DApBL2M, H101) induced seizures in C57BL/6 mice to various degrees. The BeAn strain and DApBL2M mutant were similar to the DA strain in the percentages of mice developing seizures and neuropathological changes and in the extent of infected cells. The GDVII and WW strains caused 100% mortality by days 5 and 6 p.i., respectively, at which time neuropathological changes and neuronal infection were extensive. The H101 mutant induced seizures and caused 100% mortality by day 7 p.i.; however, only minor neuropathological changes and few infected cells were observed. Thus, in H101 mutant infections, it appears that elevated levels of cytokines, rather than neuronal cell death, play the dominant role in seizure induction.     

Genetic control of immune responses to the 18-kDa protein of Mycobacterium leprae. Different TH1 subsets may be involved in proliferative and delayed-type hypersensitivity responses.

In vitro and in vivo responses to the 18-kDa protein of Mycobacterium leprae have been analysed in different strains of mice. Lymphocytes from BALB/cJ (H-2d), BALB.B (H-2b), B10.BR (H-2k), and B10.M (H-2f) mice primed with 18-kDa protein yielded high T cell proliferative responses, while those from C57BL/10J (H-2b) mice yielded lower responses. Both H-2 and non-H-2 genes contributed to the magnitude of responsiveness. F1 mice from high and low responder strains showed high responsiveness to the 18-kDa protein. Supernatants from lymph node cell cultures prepared from 18-kDa protein-immunised BALB/cJ, B10.BR, and C57BL/10J mice contained IL-2 but no IL-4, indicating that activated T cells from both high and low responder mice were of a TH1 phenotype. Cell cultures from low responder C57BL/10J mice produced less IL-2 than those from high responders. The low responsiveness to the 18-kDa protein in proliferative assays might be due to a low frequency of antigen-specific T cells in the C57BL/10J mouse strain. BALB/cJ, C57BL/10J, and F1 (BALB/cJ x B10.BR) mouse strains were tested for in vivo DTH reactions to the 18-kDa protein. All strains, including C57BL/10J, were high DTH responders. Although DTH effector cells and 18-kDa protein-specific proliferative T cells belong to the TH1 subset, our data comparing high and low responder status indicate that distinct TH1 subpopulations are stimulated in response to the 18-kDa protein of M. leprae.     

Separation of T and B lymphocytes from various mouse strains by density gradient electrophoresis.

T and B mouse spleen lymphocytes were separated by density gradient electrophoresis on the basis of their surface charge. In all strains examined, the T lymphocytes were found in the high mobility fractions and the B in the low. The T and B cells were separated completely in most fractions, with some overlapping in the middle. Significant differences were found in the electrophoretic distribution profiles between the strains: C57BL/6j, C57BL/10j, (BALB/cXC57BL/6j)F1, and all the following: B6.C-H-2d/cBy (congenic to C57BL/6j), BALB/c, CBA/H/T6j, C57BL/10Sn, and C3H. The C57BL/6j and the (BALB/cXC57BL/6j)F1 cells appear more heterogeneous as far as electrophoretic mobility is concerned. Almost all the other strains give two major peaks. Moreover, the high mobility areas are less populated in the C57BL/6j and the (BALB/cXC57BL/6j)F1 animals than in all the others. The above differences were found consistently when cells prepared by different methods were electrophoresed. It is concluded that the surface charge of lymphocytes may be genetically determined. Possible dependency on the H-2 complex or non-H-2 areas is discussed.     

The main difference between the repertoire of receptors of effector T-killers and their secondary precursors (memory cells)

Receptor repertoire analysis of in vivo induced secondary cytotoxic T lymphocyte precursors (pCTL-2) was performed, using the technique of their specific adherence to macrophage monolayers with subsequent elution of the adherent pCTL-2 and their activation by heat-killed donor stimulator cells. The capacity of anti-H-2Kb pCTL-2 receptors to contact H-2Kbm has been revealed only in a minor pCTL-2 component whose progenitors were able to lyse mutant bm1 target cells (TC). Unlike poor cross-reactivity of CTL descended from anti-Kb, pCTL-2 which were eluted from the donor monolayer, CTL-progenitors of anti-Kb pCTL-2 eluted from bm 1 or B10. A (4R) third-party monolayers lyse in equal quantities the donor TC and those third-party TC from which they have been eluted, but fail to lyse other TC. Enrichment of pCTL-2 eluted from bm 1 or B10. A (4R) monolayers is 6- or 12-fold lower, respectively, than after their elution from the donor monolayer. The findings indicate that anti-class I MHC pCTL-2 are separated into fractions, with their receptors being strongly specific (with high affinity) to the particular fragment of the same complex epitope without cross-reactivity to other fragments. These data differentiate pCTL-2 receptors from effector CTL ones which are homogenous in specificity to a whole (single) complex epitope with variable degree of complementarity. A cardinal distinction of receptor repertoire between CTL, pCTL-2 and suppressor T cells specific to the same class I MHC molecule and alteration of the active site during pCTL-2 differentiation have been suggested.     

Separation of T and B lymphocytes from various mouse strains by density gradient electrophoresis

T and B mouse spleen lymphocytes were separated by density gradient electrophoresis on the basis of their surface charge. In all strains examined, the T lymphocytes were found in the high mobility fractions and the B in the low. The T and B cells were separated completely in most fractions, with some overlapping in the middle. Significant differences were found in the electrophoretic distribution profiles between the strains: C57BL/6j, C57BL/10j, (BALB/cXC57BL/6j)F₁, and all the following: B₆·C-H-2^d/cBy (congenic to C57BL/6j), BALB/c, CBA/H/T6j, C57BL/10Sn, and C3H. The C57BL/6j and the (BALB/cXC57BL/6j)F₁ cells appear more heterogeneous as far as electrophoretic mobility is concerned. Almost all the other strains give two major peaks. Moreover, the high mobility areas are less populated in the C57BL/6j and the (BALB/cXC57BL/6j)F₁ animals than in all the others. The above differences were found consistently when cells prepared by different methods were electrophoresed. It is concluded that the surface charge of lymphocytes may be genetically determined. Possible dependency on the H-2 complex or non-H-2 areas is discussed.     

Genetic control of murine T cell proliferative responses to Mycobacterium leprae. V. Evidence for cross-reactivity between host antigens and Mycobacterium leprae

T cell proliferative responses to Mycobacterium leprae were measured by immunization of mice at the base of the tail with Ag and challenging lymphocytes from draining lymph nodes in culture with M. leprae. C57BL/10J and B10.BR mice were identified as low responder mice and the congenic strains B10.M, B10.Q, and B10.AKM as high responders whereas F1 (high x low) hybrid mice were found to be low responders. The cellular basis of low responsiveness did not appear to result from a defect in Ag-presenting cells or the activation of suppressor T cells by M. leprae. The influence of the environment in which T cells developed on responsiveness to M. leprae was analyzed in chimeric mice prepared by irradiating F1(C57BL/10J x B10.M) mice and reconstituting with bone marrow from C57BL/10J, B10.M, or F1 donors. Six weeks later, chimeric mice were immunized with M. leprae, lymph node cells were subsequently prepared, and H-2 phenotyped and challenged in culture with M. leprae Ag. T cell proliferative responses were found to be low in all cases, similar to those observed using lymph node cells from F1 hybrid mice. These results suggested that high responder B10.M lymphocytes developing in the irradiated F1 mice became tolerized to antigenic determinants found on M. leprae. This implied cross-reactive epitopes existed between some mouse strains and M. leprae. Low responsiveness to M. leprae in low responder and F1 hybrid mice may result from tolerance to H-2-encoded Ag that show cross-reactivity with M. leprae.     

Genetic control of acquired resistance to visceral leishmaniasis in mice

A series of H-2 and non-H-2 congenic resistant (CR) strains on a C57BL/10Sn background were infected with 10(7) amastigotes of Leishmania donovani. Non-H-2 congenic strains B10.LP-H-3b and B10.CE(30NX) and (B10.LP-H-3b x B10)F1 hybrids showed a very rapid decrease in liver-parasite burdens beyond day 21. Parasite counts for these strains at day 35 were significantly lower than for all other strains tested. The rapid decrease in parasite numbers, massive lymphocellular infiltration into the liver and strong delayed hypersensitivity reactions to parasite antigens in strains congenic for a portion of chromosome 2 indicated that acquired immunity to L. donovani was controlled by a dominant gene at or near the Ir-2 locus. In addition, B10.129(10M) mice, which differ from C57BL/10Sn at the H-11 locus, showed highly significant increases in parasite numbers at day 35. Other observations supporting the absence of acquired immunity in B10.129(10M) included negative delayed hypersensitivity tests to parasite antigens and the absence of lymphocellular infiltrate into the liver. Although the differences were not as pronounced, H-2 CR strains with H-2b, H-2a, and H-2k haplotypes also showed significantly greater decreases in parasite numbers by day 35 as compared to other H-2 CR strains.     

Xenotropic virus-related restriction patterns of non-H-2 histocompatibility mutant mice strains

The relationship between alteration in the number of xenotropic virus-related sequences and non-H-2 histocompatibility (H) mutations in mice was investigated. Mutant classifications included gain, loss, and loss-gain mutations. Genomic DNA from a panel of non-H-2 H mutant strains on the C57BL/6 and BALB/c backgrounds was digested with a set of restriction enzymes with varying numbers of sites within endogenous xenotropic-related sequences. The digested DNA was then resolved on agarose gels. Southern blots of digested DNA were hybridized with the pX_env probe specific for the env sequence of xenotropic viral sequences. The number of hybridizing bands varied from 7 to 19, depending on the restriction enzyme and inbred background. Most mutant strains were identical in their restriction patterns to the respective background strains. However, two B6 mutant strains, KH84 and HZ54, differed from C57BL/6 at a single band which appeared to be inherited from BALB/c in the derivation of the two congenic strains. The HZ43 strain lacked a male-specific band shared by both C57BL/6 and BALB/c; this loss was evidently independent of the original mutation which was observed to be autosomal. However, the KH148B and KH84 strains on the C57BL/6 background lacked single B6 bands. Both mutants were classified as gain mutants. An examination of previous reciprocal graft rejection patterns and retrovirus linkage to non-H-2 H loci indicated a strong inverse relationship between a linked retroviral sequence and presentation of a non-H-2 H antigen. This inverse correlation is consistent with reports of gene inactivation following retroviral insertion.     

Immune islet killing mechanisms associated with insulin-dependent diabetes: in vitro expression of cellular and antibody-mediated islet cell cytotoxicity in humans

In previous work we have shown that some bacteria can bind to human lymphocytes and can be used to identify lymphocyte subpopulations in conventionally stained blood smears. These bacteria are of different species or genera, which makes it difficult to study the binding mechanism. Also, the main marker for B cells, Brucella melitensis, is of very small size and highly pathogenic. Here we show that B cells as well as some of the T cell subpopulations can be identified by different mutants obtained from a strain of an Escherichia coli. Two procedures were used to generate mutants. First, E. coli-YS57 (pro-his-trp-) was mutagenized with N-methyl-N'-nitro-N-nitrosoguanidine and the binding to mouse spleen cells was used as a selective pressure. Second, phage-resistant mutants of E. coli-YS57 were obtained and tested for the ability to bind to lymphocytes. Out of 10 strains selected by the former procedure, 5 bound to a significant number of human lymphocytes. All four phage-resistant mutants bound to human lymphocytes. Out of the total of nine mutants that bound to lymphocytes, six bound consistently, i.e., they bound to similar percentages of peripheral blood lymphocytes from different normal donors. One phage-resistant mutant, E. coli USC-106, bound only to B cells. The subpopulations of lymphocytes identified by the mutants were essentially the same as those identified by different species or genera of bacteria. We concluded that E. coli mutants can be obtained that identify human lymphocyte subpopulations and that one of these mutants recognizes B cells; these mutants may be used to study the nature of the receptors for bacteria on lymphocytes, which appear to have a lectin-like nature.     

Analysis ofH-2 mutants: Evidence for multiple CML target specificities controlled by theH-2K b gene

C57BL/6 (H-2 ^b ) mice and two mutants derived from this strain, B6.C-H-2 ^ba (Hz1) andE6-H-2 ^bd (M505), were studied in a number of functional tests, in vitro and in vivo, that assay for differences at theH-2 complex. All three strains give rise to reciprocal mixed lymphocyte reactivity (MLR) and cell-mediated lympholysis (CML) in vitro as well as graft-host reactivity (GVHR) and skin graft rejection in vivo. Analysis for cross-reactivity between these strains in CML revealed that the gained antigens in each mutant do not cross-react, and that Hz1 has lost an antigen shared by C57BL/6 and M505 strains. In addition, spleen cells from B10.A(4R) mice, which differ from theH-2 ^b haplotype only at theK end of theH-2 complex, recognize a common antigen shared by all three strains tested. Provided that the mutations occurred in theH-2K ^b gene, these data indicate that a) there are at least three antigenic specificities coded for by theH-2K ^b gene(s) that serve as targets for receptors on thymus-derived (T) cells in CML; b) since C57BL/6 strain mice and the mutants are serologically indistinguishable on a qualitative basis, the antigens recognized by the receptors on T cells and by humoral H-2 antibody are nonidentical; and c) mutation in theH-2K ^b locus itself can give rise to allogeneic recognition phenomena such as MLR and GVHR.     

Liver tissue graft rejection in murine major histocompatibility complex mutants

Liver tissue grafts between seven H-2 mutants and their parental strains have been studied. Each of these mutants was originally identified by reciprocal mutant—parental strain skin graft rejection. However, liver grafts among mutants and parental standard strains are not uniformly rejected. Liver graft rejection also fails to correlate with mutant—parental stimulation in CML and MLC. In addition, the immune reaction pattern of female mutant animals against grafts of male liver differs from the reaction pattern found in parental standard strains. Several explanations for the differences between immune response to liver and skin grafts are proposed, including different T cell subsets involved in recognition, availability of antigenic sites to immunocompetent cells, and structural differences between mutant and parental H-2 antigens. Abbreviations used in this paper: bml, 2, 3, 4,14; dml; fm2=mutants of strains C57BL/6, B10.D2 and B10.M respectively; B6=C57BL/6     

Mouse hepatitis virus 3 pathogenicity expressed by a lytic viral infection in bone marrow 14.8+ mu+ B lymphocyte subpopulations

Mouse hepatitis virus type 3 (MHV3) provides an excellent model for studying viral-B lymphocyte interaction in the immune system, which plays an important role in the outcome of an acute disease. Bone marrow B lymphocyte subpopulations, at various times postinfection, were studied in genetically C57BL/6 and resistant A/J mice, infected with pathogenic L2-MHV3 and its nonpathogenic variant, YAC-MHV3. B lineage cell subpopulations were identified by double immunofluorescence assays using mAb of terminal deoxynucleotidyl transferase, 14.8 and cytoplasmic (cu) or surface (su) Ig mu-chains. Results revealed diminished percentage and absolute number in the bone marrow 14.8+ mu+ B lymphocyte subpopulations, including pre-B (cu+ su-) and B (cu+ su+) cells of L2-MHV3-infected susceptible C57BL/6 mice; whereas, slight or no increase was evident in the cell subpopulations of L2-MHV3 infected resistant A/J mice or in YAC-MHV3 infected in both strains of mice. Abnormal large-sized forms of the 14.8+ mu+ cells occurred, at 48-h postinfection, in L2-MHV3-infected susceptible C57BL/6 mice only. In contrast, no change in the percentage and absolute number of precursor cells (terminal deoxynucleotidyl transferase positive) and pre pre-B cells (14.8+ mu-) were detected in all infected mice. In vitro L2-MHV3 infection of C57BL/6 bone marrow purified B lineage cell subpopulations showed that pre-B (cu+ su-) and B (cu+ su+) cells became abnormally large in size and depleted in number as a result of a productive and lytic viral replication. Low L2-MHV3 viral replication occurred in these cell subpopulations of A/J mice but no YAC-MHV3 virus was produced in the cells of both strains of mice. Pre pre-B (14.8+ mu-) cells in both strains were not permissive to L2-MHV3 or YAC-MHV3 viral replication. These results are discussed with regard to the role of humoral immunodeficiency in the pathogenic process.     

Modification of survival rate of mouse embryos developing in heterozygous females for ovum mutant gene

The DDK syndrome (polar infertility) is caused by an incompatibility system due to the ovum mutant (Om) locus. For brevity, the following gene symbols are used in the present report: DDK allele, Om; C57BL/6Cr allele, +. In this investigation, we first attempted to introduce the Om allele of DDK strain into the genetic background of C57BL/6Cr strain. The attempt resulted in the production of no young at the third generation of successive backcrosses. Secondly, mating experiments were performed with heterozygous (Om/+) females having background genes of C57BL/6Cr and DDK strains in the ratios 1:1(B1D), 3:1(B3D), 7:1(B7D), and 15:1(B15D). The survival rate of the embryos as judged by the percentage number of live fetuses/number of corpora lutea at Day 12 of pregnancy was 41.3 +/- 3.2%, 27.3 +/- 3. 2%, 16.4 +/- 3.3%, and 11.3 +/- 3.2% (mean +/- SEM) in the B1D, B3D, B7D, and B15D females, respectively, when they were mated with C57BL/6Cr males. Furthermore, the increased embryonic mortality in the heterozygous (Om/+) females with more background genes of C57BL/6Cr strain was found to be due to a failure in blastocyst formation, as in the DDK syndrome. The parallelism between the proportion of C57BL/6Cr background genes and embryonic mortality has led to a hypothesis proposing the participation of a modifier gene, namely that a mechanism similar to allelic exclusion may be working in the synthesis of cytoplasmic factor of eggs and that only the Om allele is activated during oogenesis to produce DDK-type cytoplasmic factor in heterozygous (Om/+) females having a modifier gene in the homozygous state.     

Interaction of Acholeplasma laidlawii and Mycoplasma arthritidis with the lymphocytes of mice of different strains

The interaction of mycoplasmas and mouse lymphocytes has been studied by the microbiological and electron-microscopic methods. The experiments have shown that A. laidlawii and M. arthritidis are adsorbed on lymphocytes and thymocytes of (C57BL6 X A/He)F1, BALB and C57BL mice after 15 minutes of their joint incubation at 37 degrees C, 1 hour later adsorption reaches its maximum intensity and after further prolongation of the time of incubation the number of adsorbed microbial cells remains unchanged. The first stage of the interaction of mycoplasmas with splenic and thymic lymphocytes (adsorption) is the same in (C57BL6 X X A/He)F1, BALB and C57BL mice, and differences in the persistence of mycoplasmas in mice of the above strains are probably due not to different capacity of the cells for adsorbing mycoplasmas, but to differences in the immune status of these animals.