Disease relevance of Igh-1a

• Clinically observable keratitis began 10 days postinoculation in susceptible C.AL-20 (Igh-1d) and moderately susceptible BALB/c (Igh-1a) mice, whereas HSV-1-resistant C.B-17 (Igh-1b) mice rarely developed disease [1].
• Eighty-two percent of C.AL-20 (Igh-1d) mice, 40% of BALB/cByJ (Igh-1a) mice and 12% of the C.B-17 (Igh-1b) mice developed herpes simplex keratitis (HSK) following corneal challenge with 2.5 X 10(4) PFU HSV-1 strain KOS [2].
• Igh-1-disparate congenic murine strains differ in their susceptibility to develop contralateral chorioretinitis after intracameral (AC) inoculation with Herpes simplex virus type 1 (HSV-1): 75% of BALB/cByJ (Igh-1a) and 5% of C.B-17 (Igh-1b) develop necrotizing chorioretinitis [3].
• Following intracameral inoculation of 1.5 x 10(4) PFU HSV-1 (KOS), 100% of BALB/c (Igh-1a), 62% of A/J (Igh-1e) and none of the C57BL/6J (Igh-1b) inbred mice developed contralateral necrotizing chorioretinitis [4].
• Igh-linked genes that influence BCG-induced splenomegaly were located on the centrometric side of the Igh-1 locus [5].

High impact information on Igh-1a

• The suppression induced by this monoclonal T-cell product is restricted by both H-2 and Igh-1 genes whereas anti-HEL antibodies bearing a predominant idiotype are induced in all mice strains tested, irrespective of their H-2 haplotype or Igh-1 allotype [6].
• A family of T-cell alloantigens linked to Igh-1 [7].
• Interestingly enough, total IgA and IgG2a levels also were higher in Igh-1a than in Igh-1b strains [8].
• The specificity of RF was apparently further controlled by genes linked to but different from the Igh-C locus, as indicated by the absence of IgG2aa-specific RF in one of the 6 Igh-1a strains tested [8].
• Tthyd, a new thymocyte alloantigen linked to Igh-1. Implications for a switch mechanism for T cell antigen receptors [9].

Biological context of Igh-1a

• In order to verify whether the gamma 2a-related isotypic genes, namely gamma 2c and gamma 2a, could correspond to those present as alleles in domestic mice (Igh-1b and Igh-1a), a genomic library from Mus m.musculus strain (MAI) was constructed [10].
• Gene conversion by the corresponding gamma 2b gene has been proposed to explain the multiple differences between the nucleic acid sequences of BALB/c (Igh-1a) and C57BL/6 (Igh-1b) gamma 2a immunoglobulin allelic genes [10].
• These mice possess two CH2 IgH-1b and two CH2 Igh-1a/CH2 Igh-1d determinants, suggesting that these variant immunoglobulin arose from recombinations within the CH2 domain [11].
• Genetic analysis between high hapten-augmentable plaque production and allotypes in the (129/J X B6) crosses of the same H-2b haplotypes revealed that all of the backcrosses and F2 with high hapten-augmentable plaque production had the Igh-1a allele of the high-producer, 129/J mouse [12].
• The anti-CII antibody response stimulated by Ab2 was observed in DBA/1J (H-2q, Igh-1c) and DBA/2 (H-2q, Igh-1c) mice, but not in the BALB/c (H-2d, Igh-1a) and C57BL/6 (H-2b, Igh-1b) strains, thereby suggesting that the anti-CII antibody response elicited by Ab2 is controlled by the Igh gene [13].

Anatomical context of Igh-1a

• Anterior chamber inoculation resulted in contralateral retinal necrosis in 75% of BALB/c (Igh-1a) mice, 30% of C.AL-20 (Igh-1d) and 5% of the C.B-17 (Igh-1b) congenic mice; all strains showed ipsilateral retinal sparing [4].
• B cells as well as macrophages served as an effective presentation template for the photoTCSA-SC sensitization in the high responder Igh-1a mice, whereas B cells failed in inducing the CPS reaction in the low responder Igh-1d mice [14].
• The linkage to Igh-1 allotype of the T cell products was established by testing with Igh-1-congenic strains with different backgrounds including the H-2 complex [15].
• The Igh1 allotype distribution in the bone marrow and spleen plasma cells showed a large variation in the Igh1a/Igh1b ratio among old individual mice and often also between bone marrow and spleen within a single animal with or without a H-Ig component [16].
• The in vivo suppression was specific for Igh-1b+ B cells as the recipients' levels of Igh-1a and Igh-4b (IgG1b) were unaffected [17].

Associations of Igh-1a with chemical compounds

• The influence of Igh-1 genes on the class and subclass distribution of oxazolone-specific antibodies [18].

Regulatory relationships of Igh-1a

• Furthermore, they suggest that the 11-5 IdX markers identified are shared by alloantibodies of the BALB/c (Igh1a) and A.TH (Igh1e) mouse strains and may be expressed independently of Igh-C allotype markers [19].

Other interactions of Igh-1a

• We found new allotypes of the Igh-1 and Igh-4 loci [11].
• To determine the origin of anti-DNA antibodies, experiments were conducted whereby newborn BALB/c (Igh-1a) mice were injected with F1 cells from mice resulting from a crossing between Igh congenic BALB/c mice bearing the IgCHb allotype and conventional C57BL/6 mice (Igh-1b) [20].
• Idiopathic paraproteinaemia V. Expression of Igh1 and Igh5 allotypes within the homogeneous immunoglobulins of ageing (C57BL/LiARij X CBA/BrARij)F1 mouse [16].
• Spleen cells from naive HSK-susceptible CAL-20 (Igh-1d) and BALB/c (Igh-1a) mice lysed YAC-1 targets better than HSK-resistant C.B-17 (Igh-1b) mice [21].
• Furthermore, nucleotide sequence comparisons reveal that the region encompassing the site of germline Igh-8 transcription initiation is highly homologous to part of the Ig2b exon, and is also conserved upstream of the Igh-1 switch region [22].

Analytical, diagnostic and therapeutic context of Igh-1a

• The synthesis and clonal diversity of IgG2a molecules bearing the paternally inherited immunoglobulin allotype have been examined in the offspring of matings between BALB/c mothers (Igh-1a) and SJL or C57BL/10 males (both Igh-1b) using a sensitive quantitative single radial immunodiffusion in gel assay and isoelectric focusing with autoradiography [23].
• Taking advantage of the different Igh1 allotypic markers between the two strains, the development of IP with increasing age was investigated by agar electrophoresis, immunoelectrophoresis and immunofixation [24].

References