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1.
Starch gel electrophoresis and histochemical staining with l-leucyl-l-tyrosine have revealed genetic variation for dipeptidase in Rattus norvegicus. The tissue distribution, substrate specificity, and heterozygous expression as a monmeric protein suggest homology of the variant peptidase to human PEP-C and mouse Pep-3 (Dip-1). We propose Peptidase-3 (Pep-3) as a name for this autosomal locus in the rat. The allele responsible for slower (less anodal) electrophoretic migration is designated Pep-3 a and is characteristic of strain ACI/Pit. A faster (more anodal) electrophoretic mobility is the product of the Pep-3 b allele in strain F344/Pit. Twenty-five additional inbred strains carry Pep-3 a and 16 others carry Pep-3 b . Wild rats trapped in Pittsburgh were polymorphic for this locus. Alleles at Pep-3 segregated independently of c (linkage group I), a (linkage group IV), RT2 and Es-1 (linkage group V), h (linkage group VI), and RTI (linkage group VIII). 相似文献
2.
A genetic locus controlling the electrophoretic mobility of an acid phosphatase in the rat (Rattus norvegicus) is described. The locus, designed Acp-2, is not expressed in erythrocytes but is expressed in all other tissues studied. The product of Acp-2 hydrolyzes a wide variety of phosphate monoesters and is inhibited by l(+)-tartaric acid. Inbred rat strains have fixed either allele Acp-2a or allele Acp-2b. Codominant expression is observed in the respective F1 hybrids. Backcross progenies revealed the expected 1:1 segregation ratio. Possible loose linkage was found between the Acp-2 and the Pep-3 gene loci at a recombination frequency of 0.36±0.06.Supported by the Deutsche Forschungsgemeinschaft (Grant Be 352/15) and by a grant from the Alexander-von-Humboldt-Stiftung (VB2-FLF). 相似文献
3.
Using a pair of congenic strains of mice differing only at the Mls haplotype (Mls locus and closely linked genes), BALB/c (Mls
b
) and BALB.D2-Mls
a
, we have compared the in vitro proliferative responses of M1sb lymphocytes to M1sa antigens presented on either lymph node cells (LNC) or peritoneal adherent cells (PAC). Results showed that M1sa-PAC are stronger stimulators than M1sa-LNC, and furthermore, that the supernatant from M1sa-PAC may be effective in eliciting a lymphocyte proliferative response. The proliferation in response to PAC supernatant is partially due to activation by nonspecific factor(s); however, the response in the presence of M1sa incompatible PAC supernatant is about three times greater than the response obtained in the presence of syngeneic M1sb-PAC supernatant, suggesting an additional stimulation by soluble M1sa antigens. Contrasting with the ability of PAC-supernatant to stimulate a primary proliferative response in vitro, the in vivo immunization of Mlsb mice with M1sa-PAC supernatant abrogates the specific proliferative response in subsequent one-way mixed lymphocyte cultures. This abrogation of the specific response is comparable to that observed after immunization with intact M1sa peritoneal or spleen cells, although in the latter case the anti-H-2 proliferative response is also decreased, regardless of whether the H-2 incompatible stimulating cells express an additional incompatibility for M1sa. The proliferation of untreated, but not of M1sa-immunized BALB/c LNC, is stronger in cultures with DBA/2 stimulating cells (incompatible for M1sa and other non-H-2 antigens) than in cultures with BALBM-Mls
a
cells (incompatible for M1sa alone), and is comparable in intensity to that activated by H-2 incompatibility. We conclude that M1sa antigens are more efficiently recognized by unprimed helper T cells when presented on PAC than when presented on LNC. In the primary proliferative response, the effects of M1sa and other non-H-2 antigens may be cumulative. In vivo immunization against M1sa antigens results in suppression of the specific proliferative response and, to a certain extent, of the nonspecific proliferative response (directed against both H-2 and other non-H-2 antigens). Since M1sa antigens are obtainable in soluble form, their physicochemical purification can now be envisaged. 相似文献
4.
A series of congenic mice on the BALB/c genetic background have been employed to localize a teratocarcinoma transplantation rejection locus, Gt-1, to the K side of the H-2 locus on chromosome 17. Previous studies have placed the Gt-1
sv allele about 8 centimorgans away from the H-2
b or H-2
bv1 locus. Teratocarcinomas derived from 129/sv mice, Gt-1
sv (H-2K
bv1/H-2D
bv1), are rejected by BALB/c (H-2K
d/H-2Dd) and BALB-G mice (H-2K
d/H2D-b, but form tumors in BALB-B (H-2K
b/H2D
b) and BALB/5R5 mice (H-2K
b/H2D
d). In the reciprocal tumor-rejection test, a BALB/c teratocarcinoma was rejected by immunized BALB·B mice, but formed tumors in the immunized isogenic BALB/c mouse. These studies demonstrate the reciprocal expression of two Gt-1 alleles, one Gt-1
c, in BALB/c mice, and the other, Gt-1
sv, in the congenic BALB·B mice. Shedlovsky and co-workers have placed the Gt-1 locus in a similar location on the K side of the H-2 locus on chromosome 17. 相似文献
5.
Mario Sanchez Borges Yoshihiro Kumagai Ko Okumura Nakami Hirayama Zoltan Ovary Tomio Tada 《Immunogenetics》1981,13(6):499-507
Two alloantisera against hybridoma-derived IgE detected allotypic determinants expressed on the murine s chain. An antiserum raised in BALB/c mice against monoclonal IgE of C57BL/6 origin reacted exclusively with IgE of strains having Igh-1b (IgG2a) allotype. The second antiserum, C57BL/6 anti-BALB/c monoclonal IgE, reacted with IgE of strains having Igh-1a, Igh-1d, Igh-1e and Igh-1j allotypes. The genetic studies of (BALB/c x C57BL/6)F1 and backcross F2 animals indicated that the locus controlling the IgE allotype is linked to the Igh-1 locus. This was further confirmed by the possession of respective IgE allotypes by Igh-C congenic mice, BALB/c and BAB-14, C3H.SW/Hz and CWB/Hz. Thus, the allotype detected on the chain is controlled by the seventh murine immunoglobulin allotype locus, and should be designated as the Igh-7 allotype.Abbreviations used in this paper PCA
passive cutaneous anaphylaxis
- RID
radioimmunodiffusion
- i.p.
intraperitoneally
- EA
egg albumin
- Igh-C
immunoglobulin heavy chain constant region locus
- DNP
2,4-dinitrophenyl
- PBS
phosphate-buffered saline
- NMS
normal mouse serum
- KLH
keyhole limpet hemocyanin
Visiting investigator supported by the Scientific and Humanistic Development Council from the Central University of Venezuela, currently at the following address: Consejo de Desarrollo Cientifico y Universidad Central de Venezuela, Av. Principal Urb. La Floresta Ota., Silenia Caracas, Venezuela. 相似文献
6.
The minor lymphocyte stimulating (Mls) locus codes for lymphocyte activating determinants (LADs) on murine B lymphocytes, but not T lymphocytes. This observation was strengthened by a series of techniques which allow deletion and addition of T and B cells. These included the use of cytotoxic antisera such as anti-Thy 1.2, anti-MTLA, anti-MBLA, and complement, and the use of a goat anti-μ antisera, and finally the use of a fluorescence activated cell sorter (FACS).The studies in this report document the organ distribution and the ontogenetic appearance of the surface LADs on the surface of B lymphocytes from DBA/2N (H-2d, Mlsa) and CBA/J (H-2k, Mlsd) mice. Adult-like ability to stimulate H-2 identical BALB/c (H-2d, Mlsb) and C3H/He (H-2k, Mlsc) responder cells appeared at about 4–5 weeks of age. Inability of neonatal cells to induce an Mls-defined MLC was found not to be due to a low frequency of B lymphocytes or to the presence of suppressor cells, but due to the absence of the Mls-coded LADs on their surface. These data support the concept that the Mls-coded LADs are present on adult B lymphocytes and are specific markers of B-cell differentiation, which is preceded by membrane IgM and the δ homologue of human IgD, Ia, and the receptor for the third component of complement. 相似文献
7.
Several strains of mice were tested for their capacity to provide immunoglobulin L chains required for the expression of the major cross-reactive idiotype (CRIA) associated with p-azophenylarsonate-specific antibodies of strain A mice. To facilitate testing, mice were bred that were homozygous for Igh-C
e
and Lyt-2
a
, 3
a
, i. e., they possessed genes controlling H chains but not L chains required for expression of the CRIA. Such male mice were mated to females of various strains and their offspring were tested; expression of CRIA indicated the presence in the female parent of genes controlling the appropriate L chains. All females bearing the Lyt-2
a
, 3
b
or Lyt-2
b
, 3
b
genotype yielded offspring, most of which were CRI
A
+
, whereas all the offspring of females that were Lyt-2
a
, 3
a
were CRI
A
–
. The female parents included mice of several strains that are congenic for Lyt-2
a
, 3
b
, Lyt-2
b
, 3
b
or Lyt-2
a
, 3
b
, thus demonstrating very close linkage between the Lyt loci and the expression of CRIA. In addition, doubly congenic strains of mice with the heavy chain allotype of the CRI
A
+
AL/N strain and the Lyt-2
a
, 3
a
genotype on a BALB/c background failed to express CRIA. The data provide further evidence for the similarity of repertoires of L chains in Lyt-3
b
mice of various strains. When genes were present controlling A/J H chains and L chains of C57BL/6 or BALB/c origin, the quantitative expression of CRIA was only slightly lower than that observed in A/J mice. Mice possessing genes controlling the H or L chains required for CRIA expression, but not both, did not express CRIA but synthesized Ar-specific antibodies which contained low but significant concentrations of the idiotype-associated chain. 相似文献
8.
Recombinant inbred strains were used to demonstrate the existence of a major locus on chromosome 1, designated Sap, which controls the endogenous concentration of the mouse acute phase reactant, serum amyloid P-component (SAP). Levels of SAP were associated with alleles at the Ly-9 locus in two sets of RI strains: BXD (C57BL/6J × DBA/2) and BXH (C57BL/6J × C3H/HeJ). Low endogenous levels of SAP were present in the C57BL/6J progenitor strain and in most of the RI strains which inherited the Ly-9
ballele. High levels of SAP were present in the DBA/2J and C3H/HeJ progenitors and in most of the RI strains which inherited the Ly-9
aallele. In the BXD strains 91% of the genetic variation of SAP levels was accounted for by segregation at the Ly-9 locus while an additional 9% was attributed to genetic factors unlinked to Ly-9. In the BXH strains the percentage of genetic variation accounted for by Ly-9 segregation was reduced to 46%, while 54% was accounted for by other genetic factors. Because of background genetic variation it was not possible to detect any crossovers between Sap and Ly-9. However, in the BXD strains the linkage between Sap and Ly-9 appears to be quite close. The B6.C-H-25
ccongenic strain, which carries a segment of BALB/c chromosome 1 including the minor histocompatibility locus H-25 on a C57BL/6By background, had the same endogenous SAP level as the BALB/c donor strain. 相似文献
9.
Immunogenicity of allogeneic immunoglobulins in mice were studied, measuring the allotype-specific antibody activity by agglutination
of allogeneic antibody-coated red blood cells. It was found that the serum from C.B-20 mice (Igh
b
, BALB/c-congenic) was uniquely immunogenic in BALB/c mice for allotype antibody response. Whereas the C57BL/6 (Igh
b
) serum was immunogenic only when heat aggregated and/or combined with adjuvant, the ultracentrifugation-deaggregated C.B-20
serum was definitely immunogenic when administered in a moderate dose (100 μl/mouse). Even more surprising was the fast that
very low doses (0.01–0.1 μl) of soluble C.B-20 serum, but not C57BL/6 serum, down regulated the allotype-specific response
effectively. Genetic analysis on congenic mice suggested that the immunogenicity is controlled by donorIgh orIgh-V(Id-C.B) inasmuch as the serum from BALB/c-congenic C.B-20 (Igh-V
b
C
b
), but not BALB/c-congenic BAB/14 (Igh-V
a
C
b
), mice was active in BALB/c mice in soluble form. Further studies showed that the Id-C.B was dominantly expressed on the
immunoglobulins of (BALB/c×C.B-20)F1 and (C56BL/6×C.B-20)F1 strains, and was originally derived from the C57BL/Ka strain. The major determinant for the antibody production was encoded
inIgh-C, but not inIgh-V. It is suggested thatId-C.B controls the allotype-specific antibody response in an unusual manner, possibly acting as a unique determinant activating
helper T cells. 相似文献
10.
BALB/cBy anti-BALB/cJ spleen cells were tested in a secondary cellmediated lympholysis assay. The effector cells generated displayed a positive cytotoxic effect against Con A lymphoblasts from only those strains that were typed serologically as having theQa-2
a allele. Confirmation that the target antigen is controlled by a locus closely associated with or identical toQa-2 was obtained by the findings that target cells from B6.K2 (Qa-2
a,Qa-3
a) mice were lysed by the effector cells, while those from theQa-2, 3 congenic strain B6.K1 (Qa-2
b,Qa-3
b) were not. The fact that target cells from aQa-2-positive/Qa-3-negative strain (DBA/1,Qa-2
ai,Qa-3
b) were killed indicates that the target antigen is controlled, at least in part, by theQa-2 locus, not the Qa-3.There is no observedH-2 genetic restriction for this cytotoxic effect, since target cells which have theQa-2
a allele but differ from the stimulator cells at theH-2K, D, andI regions were lysed efficiently. 相似文献
11.
Robert Semeonoff 《Biochemical genetics》1972,6(2-3):125-138
Three polymorphic loci have been identified in the prairie vole, Microtus ochrogaster. Together they control a group of plasma esterases which can be separated using starch gel electrophoresis. A structural locus, Es-1, produces an enzyme which from genetic evidence appears to be a dimer. The allele Es-1
a produces a wholly active subunit, and homozygotes give a single enzyme band. The product of the second allele, Es-1
o, cannot form active enzyme on its own but will dimerize with the Es-1
a subunit, giving a hybrid enzyme with a slower electrophoretic mobility than the pure Es-1
a enzyme. The third allele, Es-1
–, has no detectable product. A second structural locus, Es-2, is linked to Es-1. The allele Es-2
a produces a single enzyme band, but the second allele Es-2
– has no detectable product. A modifier locus, Me, changes the mobility of the Es-1 enzymes. Me
f is dominant over me
s, and in homozygotes for me
s the mobility is reduced.This work was supported by National Science Foundation Grant GB6273.This is contribution No. 869 from that Department. 相似文献
12.
Ruth Saison 《Biochemical genetics》1971,5(1):27-31
Erythrocytes of 119 mink, and tissue extracts of three mink, were examined for electrophoretic patterns of lactate dehydrogenase (LDH). A variant was detected at the B locus. There are two alleles, LDH-B
a and LDH-B
b; three phenotypes, LDH-Ba, LDH-Bab, and LDH-Bb; and three genotypes, LDH-B
a/LDH-Ba, LDH-Ba/LDH-Bb, and LDH-B
b/LDH-Bb. The inheritance as observed in 24 families agrees with an autosomal, codominant, two-allele system at the LDH B locus.Supported by National Research Council Grant A-4442 and the Ontario Department of Agriculture and Food. 相似文献
13.
Biochemistry and genetics of a testosterone-dependent murine serum esterase designated esterase-29 (ES-29) are described. The enzyme was identified after disc electrophoresis and subsequent staining for esterase using -naphthyl acetate as the substrate. It was inhibited by bis-p-nitrophenyl phosphate and was resistant top-chlorophenylsulphonate and hence was classified as carboxylesterase EC 3.1.1.1. The molecular mass was estimated to be about 130 kDa. It was shown that ES-29 is under the control of two independent genes. The first, termed Es-29, is suggested to be a structural locus, linked to the cluster-2 esterase loci on chromosome 8. Three alleles atEs-29, Es-29
a, Es-29b, andEs-29
care distinguished, which determine absence (SEG/1), strong activity (BALB/cJ), and low activity (MOLH/Fre), respectively. The second locus, termedMse-1 (serum esterase modifying factor), was found to be closely linked toPre-2 on chromosome 12 and is suggested to be a modifying or regulatory gene. Two alleles were distinguished,Mse-1
a(BALB/cJ) andMse-1
m(MOL3/JA, CasBgr), which determine whether ES-29 appears as a single band or a double band, respectively.Mse-1
mis dominant toMse-1
a.This work was supported by the Deutsche Forschungsgemeinschaft. This is communication No. 70 of a research program devoted to the cellular distribution, genetics, and regulation of nonspecific esterases. 相似文献
14.
Cornelia Kolb E. Weiler I. Seppälä K. Eichmann M. Kaartinen J. Pelkonen K. Karjalainen O. Mäkelä 《Immunogenetics》1979,9(1):455-463
Two congenic strains of mice were bred in Konstanz that bear theIg heavy chain allotype gene of the C57BL/6 (Ig-1
b
) in a BALB/c background genome. One line (CB-8K) underwent eight backcross generations to BALB/c before sister-brother mating was initiated. For the other line (CB-16KN) backcrossing was continued for eight further generations, then a homozygousIg-1
b
/Ig-1
b
strain was produced by sister-brother mating. Both lines were tested for four VH markers of the BALB/c and one of the C57BL parent. The CB-16KN strain expressed the C57BL marker VHNPb together with the C57BL allotype marker, and failed to express the three BALB/c markers, VHDEX, VHS117, VHphOx and VHNPa. It thus resembled the CB-20 strain.Strain CB-8K expressed the VHNPb marker of C57BL but also all the four BALB/c markers that were tested. The strain appeared more heterogeneous than the CB-16KN strain, and a subline was bred from two exceptional mice that did not express the VHNPb marker. This subline (CB-8KN) expressed the BALB/c marker VHNPa regularly, and was negative for the VHNPb marker. It thus resembles the BAB-14 line.The crossing over event thus must have happened in one of the two meioses, which led to the CB-8K line. As BAB-14 is derived in an analogous manner to a branch of the backcross of Potter and Lieberman, which ended up in CB-20, the unexpected finding is discussed that two independent crossing over events (in CB-8KN and BAB 14) within theIg heavy chain gene region have taken place at approximately the same stage of two breeding programs.Recipient of an EMBO fellowship during part of the study. 相似文献
15.
O. L. Serov 《Biochemical genetics》1973,9(2):117-130
Three electrophoretic variants of plasma esterase in the albumin zone, presumably carboxylesterase, have been demonstrated in 250 rats representing a laboratory population of Wistar rats. Electrophoretic variants of the enzyme are believed to be controlled by two codominant alleles at the autosomal locus referred to as Es-2. The variant of carboxylesterase represented by a fast-migrating single band on starch gel electrophoresis is determined by the gene named Es-2
a, whereas the slow-migrating variant, represented by two bands, is under control of the allelic gene Es-2
b. Animals with Es-2
a/Es-2
b genotype have three bands of carboxylesterase in the albumin zone. Genetically determined polymorphism of plasma esterase, presumably carboxylesterase, in the prealbumin zone was shown in both laboratory and wild populations of rats. Breeding tests suggest that the gene referred to as Es-1
a, responsible for the presence of carboxylesterase in the prealbumin zone, is inherited dominantly, whereas animals homozygous for the allele Es-1
b locked this esterase fraction. 相似文献
16.
The differential expression of H-2 specificities recognized by antibody and by cytotoxic T lymphocytes (CTL) has been studied using a clone (FY7) of the C57BL/6 leukemia cell line FBL-3 (H-2
b
/H-2
b
). Unlike C57BL/10 spleen cells, EL-4 lymphoma cells and Y57-2C leukemia cells (allH-2
b
/H-2
b
), FY7 failed to induce the primary in vitro generation of anti-H-2b CTL by (B10.A x A)F1 (H-2
a
/H-2
a
or (B10.D2 x BALB/c)F1 (H-2
d
/H-2
d
) responder spleen cells. In addition, FY7 was not lysed by, and did not competitively inhibit anti-H-2b CTL. Quantitative absorption tests with H-2Kb and H-2Db antisera revealed that FY7 expressed these antigens in quantitatively similar amounts to EL-4. The H-2Kb product of FY7 appeared to be identical with that of C57BL/10 spleen cells both in apparent molecular weight and isoelectric point. Yet FY7 failed to inhibit anti-H-2Kb CTL competitively in a cold target inhibition assay. Possible mechanisms are discussed for the lack of T-lymphocyte recognition of the H-2Kb-gene product expressed by FY7.Abbreviations used in this paper CTL
cytotoxic T lymphocytes
- MHC
major histocompatibility complex
- MLC
mixed lymphocyte culture
- PAGE
polyacrylamide gel electrophoresis 相似文献
17.
Synthesis of “reversed” methylenecyclopropane analogues of nucleoside phosphonates 6a,7a, 6b, and 7b is described. 1-Bromo-1-bromomethylcyclopropane 8 was converted to the bromocyclopropyl phosphonate 9 by Michaelis-Arbuzov reaction with triisopropyl phosphite. Base-catalyzed β-elimination and deacetylation gave the key Z- and E-hydroxymethylcyclopropyl phosphonates 10 and 11 separated by chromatography. The Mitsunobu type of alkylation of 10 or 11 with adenine or 2-amino-6-chloropurine afforded phosphonates 12a, 12b, 13a, and 13b. Acid hydrolysis furnished the adenine and guanine analogues 6a, 7a, 6b, and 7b. The E and Z configuration was assigned on the basis of NOE experiments with phosphonates 6b and 7b. All Z- and E-isomers were also distinguished by different chemical shifts of CH2O or CH2N (H4 or H4′). Significant differences of the chemical shifts of the cyclopropane C3(3’) carbons and coupling constants 3JP,C2(2’) or 3JP,C3(3’) selective for the Z- or E-isomers were also noted. Phosphonates 6a, 7a, 6b, and 7b are devoid of significant antiviral activity. 相似文献
18.
Spleen cells from NZB mice make an unexpected primary cytotoxic T lymphocyte (CTL) response to BALB/c cells in vitro. In this study, it is shown that this response is comprised of at least three independent components. These include a response to antigens recognized in association with H-2d products, a response to Qa-1b-associated antigens which is notH-2-restricted and a response directed toward antigens not associated with either H-2d- or Qa-1b-coded determinants. The last response appears to be the weakest of the three. In addition, cells from NZB F1 mice which were either homozygous (Qa-1
a
/Qa-1
a
) or heterozygous (Qa-1
a
/Qa-1
b
) forQa-1 alleles, all responded to BALB/c cells. These data suggest that the NZB CTL response to BALB/c cells is not solely dependent on antigens coded for by genes in theH-2D-Tla region for either the sensitization or effector phases of the response. The ontogeny of the NZB anti-BALB/c CTL response coincides with that of a number of B-cell abnormalities but is shown in experiments with-suppressed NZB mice to be independent of B-cell dysfunction. Studies with (NZB x B10.D2)F1 + B10.D2 mice demonstrated that the anti-BALB/cCTL response to antigens coded for outside ofQa-1 is governed by at least two genes. Finally, it is shown that another conventionallyH-2-restricted response, that to TNP-modified isologous cells, is neither significantly cross-reactive nor markedly elevated in NZB mice. — The foregoing observations suggest that some subsets of NZB T lymphocytes are intrinsically abnormal. The possibilities that the apparent hyperreactivity of NZB CTL precursors, evidenced in the response to BALB/c cells, is primary or results from the secondary effects of excess T-cell help are discussed. 相似文献
19.
Irradiation with UVB (290–320 nm) initiates a systemic immunosuppression detectable as suppression of contact hypersensitivity (CHS). We investigated susceptibility to UV suppression in reciprocal F1-hybrid and backcross mice derived from BALB/c (low susceptibility) and C57BL/6 (high susceptibility) inbred strains. CB6F1 male mice exhibited high susceptibility and B6CF1 male mice exhibited low susceptibility, indicating a major X-linked effect in the genetic control of UV immune suppression. Females of either F1 hybrid showed intermediate suppression, consistent with random X-inactivation. A model of monogenic X-linked control was not sufficient, and evidence for the action of two genetically unlinked autosomal genes was found in parental backcross animals. Both sexes of (BALB/c × CB6F1) mice showed a 1 high: 1 low ratio of phenotypes, indicating control by a major autosomal locus, Uvs1, confirmed by propagation of the high phenotype through selective backcrossing for nine generations to BALB/c. Uvs1 was not genetically linked to 12 chromosomal markers including the pigment genes b (brown) and c (albino). Backcross animals (C57BL/6 × CB6F1) showed a significant sex difference, male mice giving a 3 high: 1 low ratio of phenotypes, compatible with the action of a second autosomal locus, Uvs2, in this hybrid. The findings are compatible with a model in which high phenotype (Uvs1
b/Uvs1
b) is dominant when subjected to recessive epistatis by the X-chromosome locus Uvs3, or by the autosomal locus Uvs2. The finding of genetic control by interacting autosomal and X-linked genes is unique. Genetically determined high susceptibility to UV immunosuppression may be an important risk factor for UV-related human diseases. 相似文献
20.
Alleles of at least two loci (rig-1 and Rig-2) regulate the levels of serum immunoglobulin of the Igh-1b class and allotype in BALB/c Igb (BAB/14) and (BALB/c × BAB/14)F1 mice. The combined effect of the BALB/c alleles at these two loci is to lower Igh-1b levels significantly below those observed in other strains and below their own levels of Igh-1a in allotype heterozygous mice. The rig-1 locus is closely linked to or within the H-2 complex. Two alleles have been defined: rig-1
d and rig-1
b in H-2
d and H-2
b haplotypes, respectively. Homozygous rig-1
d d animals heterozygous for the BALB/c Rig-2 allele(s) have very low levels of Igh-1b. The designation of Rig-2 is provisional since it has not been mapped or defined as a single locus. 相似文献