The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Gene Review

Ighg2a  -  immunoglobulin heavy constant gamma 2A

Mus musculus

Synonyms: 1810060O09Rik, Ig gamma-2A chain C region, membrane-bound form, Igh-1, Igh-1a
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

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].


  1. Histology and immunohistology of Igh-1-restricted herpes simplex keratitis in BALB/c congenic mice. Opremcak, E.M., Rice, B.A., Wells, P.A., Foster, C.S. Invest. Ophthalmol. Vis. Sci. (1990) [Pubmed]
  2. Immunogenetic influence of Igh-1 phenotype on experimental herpes simplex virus type-1 corneal infection. Opremcak, E.M., Wells, P.A., Thompson, P., Daigle, J.A., Rice, B.A., Millin, J.A., Foster, C.S. Invest. Ophthalmol. Vis. Sci. (1988) [Pubmed]
  3. Viral isolation and systemic immune responses after intracameral inoculation of herpes simplex virus type 1 in Igh-1-disparate congenic murine strains. Hemady, R., Tauber, J., Ihley, T.M., Opremcak, E.M., Foster, C.S. Invest. Ophthalmol. Vis. Sci. (1990) [Pubmed]
  4. Chorioretinal disease patterns in congenic mice following intraocular inoculation with HSV-1. Opremcak, E.M., Foster, C.S., Hemady, R., Rice, B.A., Daigle, J.A., Raizman, M.B., Chung, H., Zaltas, M. Invest. Ophthalmol. Vis. Sci. (1989) [Pubmed]
  5. Genetic control of BCG-induced granulomatous inflammation in mice. Sternick, J.L., Schrier, D.J., Moore, V.L. Exp. Lung Res. (1983) [Pubmed]
  6. Monoclonal suppressor T-cell factor displaying V H restriction and fine antigenic specificity. Adorini, L., Pini, C., De Santis, R., Robbiati, F., Doria, G., Ricciardi-Castagnoli, P. Nature (1983) [Pubmed]
  7. A family of T-cell alloantigens linked to Igh-1. Spurll, G.M., Owen, F.L. Nature (1981) [Pubmed]
  8. Rheumatoid factors in 129XB recombinant inbred strains. Igh-1-linked control of allotypic and isotypic specificities. Van Snick, J., Coutelier, J.P., Van Roost, E., Guénet, J.L. J. Exp. Med. (1984) [Pubmed]
  9. Tthyd, a new thymocyte alloantigen linked to Igh-1. Implications for a switch mechanism for T cell antigen receptors. Owen, F.L., Spurll, G.M., Panageas, E. J. Exp. Med. (1982) [Pubmed]
  10. Further evidence that BALB/c and C57BL/6 gamma 2a genes originate from two distinct isotypes. Morgado, M.G., Cam, P., Gris-Liebe, C., Cazenave, P.A., Jouvin-Marche, E. EMBO J. (1989) [Pubmed]
  11. New immunoglobulin IgG allotypes and haplotypes found in wild mice with monoclonal anti-allotope antibodies. Huang, C.M., Parsons, M., Wakeland, E.K., Moriwaki, K., Herzenberg, L.A. J. Immunol. (1982) [Pubmed]
  12. Strain differences in the development of auto-anti-idiotypic antibody regulation with age: genetic linkage to the Igh-C locus. Szewczuk, M.R. Cell. Immunol. (1984) [Pubmed]
  13. Characterization of the antibody response against the type II collagen induced by anti-idiotypic antibody. Iribe, H., Tarutani, S., Koga, T. Cell. Immunol. (1990) [Pubmed]
  14. Genetic control of contact photosensitivity to tetrachlorosalicylanilide. II. Igh complex controls the sensitivity induced by photohapten-modified spleen cells but not epidermal cells. Tokura, Y., Satoh, T., Yamada, M., Takigawa, M. Cell. Immunol. (1991) [Pubmed]
  15. Heterogeneity of Igh-linked allotypic determinants expressed on functional T cell subsets as detected by monoclonal antibodies. Karasuyama, H., Kim, M., Okumura, K., Tada, T. Eur. J. Immunol. (1984) [Pubmed]
  16. Idiopathic paraproteinaemia V. Expression of Igh1 and Igh5 allotypes within the homogeneous immunoglobulins of ageing (C57BL/LiARij X CBA/BrARij)F1 mouse. Radl, J., Vieveen, M.H., van den Akker, T.W., Benner, R., Haaijman, J.J., Zurcher, C. Clin. Exp. Immunol. (1985) [Pubmed]
  17. Igh-1b-specific CD4+CD8- T cell clones of the Th1 subset selectively suppress the Igh-1b allotype in vivo. Bartnes, K., Hannestad, K. Eur. J. Immunol. (1991) [Pubmed]
  18. The influence of Igh-1 genes on the class and subclass distribution of oxazolone-specific antibodies. László, G., Rajnavölgyi, E., Andó, I., Gergely, J. Immunogenetics (1985) [Pubmed]
  19. Idiotypic analysis of anti-I-Ak monoclonal antibodies. II. Detection of shared idiotopes on syngeneic BALB/c and allogeneic A.TH-derived anti-I-Ak mAb by BALB/c-derived anti-I-Ak anti-idiotypic mAb. Devaux, C.A., Phillips, M.L., Delovitch, T.L. J. Immunol. (1984) [Pubmed]
  20. Autoimmunity after induction of neonatal tolerance to alloantigens: role of B cell chimerism and F1 donor B cell activation. Luzuy, S., Merino, J., Engers, H., Izui, S., Lambert, P.H. J. Immunol. (1986) [Pubmed]
  21. Natural killer cellular cytotoxicity against herpes simplex virus-infected cells in Igh-1-disparate mice. Tamesis, R.R., Foster, C.S. Invest. Ophthalmol. Vis. Sci. (1990) [Pubmed]
  22. Structure and expression of mouse germline immunoglobulin gamma 3 heavy chain transcripts induced by the mitogen lipopolysaccharide. Gerondakis, S., Gaff, C., Goodman, D.J., Grumont, R.J. Immunogenetics (1991) [Pubmed]
  23. Quantitative and spectrotypic analysis of paternal IgG2a expression in normal and allotype-suppressed mice. Appleby, P., Catty, D. Immunology (1985) [Pubmed]
  24. Idiopathic paraproteinaemia. IV. The role of genetic factors in the development of monoclonal B cell proliferative disorders--a study in the ageing C57BL/KaLwRij and CBA/BrARij mouse radiation chimeras. Radl, J., Heidt, P.J., Knaan-Shanzer, S., van Zwieten, M.J. Clin. Exp. Immunol. (1984) [Pubmed]
WikiGenes - Universities