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Gene Review

Ighg2c  -  immunoglobulin heavy constant gamma 2C

Mus musculus

Synonyms: Igh-1b
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Disease relevance of Igh-1b

  • Splenocytes from both HSK-susceptible C.AL-20 (Igh-1d) and HSK-resistant C.B-17 (Igh-1b) mice mediated equal amounts of ADCC to HSV-infected cell targets using monoclonal antibodies against HSV-1 glycoprotein D. Natural killer cell activity was significantly greater in C.AL-20 than in C.B-17 splenocytes [1].
  • In contrast to NP-induced delayed-type hypersensitivity responses, which only display 4-hydroxy-5-iodo-3-nitrophenyl acetyl (NIP) cross-reactivity in Igh-1b-bearing mice, cross-reactive CS responses can also be elicited in NP-primed mice carrying the Igh-1d, Igh-1e, or Igh-1f allotypes [2].
  • Dorf and colleagues (1-4) found that the contact sensitivity (CS) primed with (4-hydroxy-3-nitrophenyl)acetyl (NP) could be elicited as easily with the iodoanalog (NIP) as with NP when studied in Igh-1b mice but could only be elicited with NP, not NIP, in Igh-1j mice [3].
  • 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 [4].
  • 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 [5].

High impact information on Igh-1b

  • Treated homozygous Ighb/b mice developed, as of 16-24 wk of age, a chronic suppression of Igh-1b expression (IgG2a of Ighb haplotype) [6].
  • In vivo treatment with cytotoxic anti-CD4 or anti-CD8 mAb of mice subjected to chronic Igh-1b suppression clearly showed that CD8+ lymphocytes (suppressor or cytotoxic cell) were essential for the maintenance of the suppression [6].
  • This anti-CD8 in vivo treatment was shown to have no effect on thymus but to severely reduce the percentages of CD8+ cells in spleen and in peripheral blood without affecting the percentages of CD4+ cells, leading to a large and rapid Igh-1b expression (up to 0.5 mg per ml of serum, the day after the end of the treatment) [6].
  • Interestingly enough, total IgA and IgG2a levels also were higher in Igh-1a than in Igh-1b strains [7].
  • The alloantiserum was raised in BALB/c (H-2d, Igh-1a) mice hyperimmunized with spleen cells of Igh allotype congenic mice, CB-20 (H-2d, Igh-1b) [8].

Biological context of Igh-1b

  • 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 [9].
  • In addition, in vivo these monoclonal antibodies modified anti-SRBC antibody production only in Igh-1b allotype-bearing mice [10].
  • With the exception of one allotope located in the hinge region of Igh-1b, all other 23 allotopes examined were preserved upon reduction and alkylation of immunoglobulin antigens [11].
  • Genetic studies of determinants recognized by these monoclonal antibodies have also suggested that the distinct Ct molecules of TsF and TaF are encoded by two discrete genes linked to the Igh-1b genes, which are located on the right side of the variable genes of Igh on the 12th chromosome [12].
  • Abrogation of Igh-1b suppression by in vivo anti-CD8 mAb treatment was achieved in adult Igha/b heterozygotes but with a lower efficiency than in adult Ighb/b homozygotes, all being chronically Igh-1b suppressed [13].

Anatomical context of Igh-1b

  • Monoclonal alloantibodies for T cell allotypic determinants were obtained by hybridizing SP-2 tumor cells with BALB/c (H-2d, Igh-1a) spleen cells, which had been repeatedly immunized with Con A-stimulated CB-20 (H-2d, Igh-1b) spleen cells [10].
  • Dendritic cells, macrophages, and B cells were purified from the spleens of Igh-1b mice [14].
  • They also did not stain a (T,G)-A--L-specific helper T cell line derived from CWB (H-2b, Igh-1b) mice, which differ from C3H.SW mice only in their heavy chain allotypes [15].
  • Bone marrow cells and B splenocytes from Igh-1b-suppressed adult Igha/b mice were shown to be able to durably express Igh-1b when transferred into irradiated Igha/a BALB/c hosts whereas whole spleen cells from such donors failed to do it [13].
  • Suppression of Igh-1b anti-sheep red blood cell plaque-forming cells was measured as late as 4 wk after the injection of allotype heterozygous (Igha/b) spleen cells, antiserum, and sheep red blood cells [16].

Associations of Igh-1b with chemical compounds


Regulatory relationships of Igh-1b

  • Exposure to either anti-CD8 or anti-CD4 mAb in vitro or in vivo leads to loss of the capacity of Ts to induce Igh-1b allotypic suppression [13].

Other interactions of Igh-1b

  • Segregation analysis with 52 recombinant inbred strains confirmed the close linkage of Igh-Gte idiotype with Igh-1b locus [18].
  • Homozygous rig-1d animals heterozygous for the BALB/c Rig-2 allele(s) have very low levels of Igh-1b [19].
  • The RF bound specifically to the MRL gamma 2 a allotype (Igh-1j) but not to the B6 gamma 2a allotype (Igh-1b) [20].

Analytical, diagnostic and therapeutic context of Igh-1b

  • An indirect asymmetrical sandwich ELISA using anti-allotype antibodies for the specific and quantitative measurement of mouse IgG2a of Igh-1b allotype [21].
  • 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 [22].


  1. Antibody-dependent cellular cytotoxicity against cells infected with herpes simplex virus type 1 in Igh-1 disparate congenic mice. Tamesis, R.R., Rodriguez, A., Hoang-Xuan, T., Foster, C.S. German journal of ophthalmology. (1993) [Pubmed]
  2. Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. VI. Evidence for different T cell receptors in cells that mediate H-21-restricted and H-2D-restricted cutaneous sensitivity responses. Sunday, M.E., Benacerraf, B., Dorf, M.E. J. Exp. Med. (1980) [Pubmed]
  3. Fine-specificity of the contact sensitivity to 4-hydroxy-3-nitrophenyl acetyl (NP). Matoso-Ferreira, A., Mäkelä, O. J. Immunol. (1983) [Pubmed]
  4. 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]
  5. 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]
  6. Cellular induction of chronic allotype suppression of IgG2a in Ighb/b homozygous mice and its abrogation by in vivo treatment with anti-CD8 monoclonal antibody. Benaroch, P., Georgatsou, E., Bordenave, G. J. Exp. Med. (1988) [Pubmed]
  7. 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]
  8. Two distinct allotypic determinants on the antigen-specific suppressor and enhancing T cell factors that are encoded by genes linked to the immunoglobulin heavy chain locus. Tokuhisa, T., Taniguchi, M. J. Exp. Med. (1982) [Pubmed]
  9. 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]
  10. T cell allotypic determinants encoded by genes linked to the immunoglobulin heavy chain locus. I. Establishment of monoclonal antibodies against allotypic determinants. Aihara, Y., Tadokoro, I., Katoh, K., Minami, M., Okuda, K. J. Immunol. (1983) [Pubmed]
  11. Structural characterization of mouse immunoglobulin allotypic determinants (allotopes) defined by monoclonal antibodies. Parsons, M., Oi, V.T., Huang, C.M., Herzenberg, L.A. Immunogenetics (1983) [Pubmed]
  12. Monoclonal alloantibodies specific for the constant region of T cell antigen receptors. Tokuhisa, T., Komatsu, Y., Uchida, Y., Taniguchi, M. J. Exp. Med. (1982) [Pubmed]
  13. T cell-induced Ig allotypic suppression in mice. II. Both CD4+ CD8- and CD4- CD8+ T cell subsets from sensitized Igha mice are required to induce suppression of Igh-1b allotype expression. Benaroch, P., Bordenave, G. J. Immunol. (1989) [Pubmed]
  14. Self gamma2a(b) protein is presented in vivo by gamma2a(b) B cells but not by dendritic cells. Granucci, F., Foti, M., Cossarizza, A., Ricciardi-Castagnoli, P. J. Immunol. (1997) [Pubmed]
  15. Cross-reactive idiotypic determinants on antibodies and antigen-specific helper T cell continuous lines. Lifshitz, R., Apte, R.N., Mozes, E. J. Immunol. (1983) [Pubmed]
  16. Generation in vivo of non-T suppressor cells with the use of anti-allotype antibody. Gilbert, K.M., Dresser, D.W. J. Immunol. (1988) [Pubmed]
  17. 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]
  18. Idiotypic analysis of anti-GAT antibodies. IX. Genetic mapping of the Gte idiotypic marker within the Igh-V locus. Ju, S.T., Dorf, M.E. J. Immunol. (1981) [Pubmed]
  19. Regulation of the production of murine IgG2a by an H-2-linked gene and other unlinked genes. Dowsett, A.P., Herzenberg, L.A., Herzenberg, L.A. Immunogenetics (1981) [Pubmed]
  20. An isotype switched and somatically mutated rheumatoid factor clone isolated from a MRL-lpr/lpr mouse exhibits limited intraclonal affinity maturation. Jacobson, B.A., Sharon, J., Shan, H., Shlomchik, M., Weigert, M.G., Marshak-Rothstein, A. J. Immunol. (1994) [Pubmed]
  21. An indirect asymmetrical sandwich ELISA using anti-allotype antibodies for the specific and quantitative measurement of mouse IgG2a of Igh-1b allotype. Klein-Schneegans, A.S., Kuntz, L., Fonteneau, P., Loor, F. J. Immunol. Methods (1989) [Pubmed]
  22. Quantitative and spectrotypic analysis of paternal IgG2a expression in normal and allotype-suppressed mice. Appleby, P., Catty, D. Immunology (1985) [Pubmed]
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