Immune status of a μ, χ transgenic mouse line. Deficient response to bacterially related antigens

Academic Article

Abstract

  • We have examined the immune repertoire and immune response of a mouse that carries transgenes for a μ heavy chain and ϰ light chain. The expression of these genes is under the regulation of their own controlling elements. The transgenes are expressed early in ontogeny and are easily detectable from day 13 of gestation onwards. The pre‐B cells seem to function normally as they generate IgM‐secreting colonies at normal frequencies. Colonies show predominantly the transgenic specificity. Expression of the transgenes is not limited to B cells since around 10%–20% of peripheral T cells and 50% of thymocytes express the μ transgene as an intracellular protein. Ectopic expression of ϰ was not seen. The spleen size of the transgenic mouse is decreased by around 20%; this reduction is largely caused by a reduction of the B cell pool. Almost all B cells express the transgenes, only 30% co‐express endogenous heavy chain genes and all co‐express endogenous light chain genes. Serum Ig levels for IgM and IgA were normal, 20% of the IgM consist of the transgenic product. Serum IgG levels were decreased. T cell functions (helper and cytotoxic) were normal. Immune responses to conventional antigens were impaired, especially in the early phases of the immune response, but after boosting they were virtually normal, except for IgG3 which remained low. Primary antibody reponses to T cell‐independent antigens of the class II type (bacterially related antigens) were absent, although precursor frequencies for these antigens were within the expected range. The significance of this finding, as it relates to allelic exclusion of Ig genes, is discussed. Copyright © 1989 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim
  • Published In

    Digital Object Identifier (doi)

    Author List

  • Lamers MC; Vakil M; Kearney JF; Langhorne J; Paige CJ; Julius MH; Mossmann H; Carsetti R; Köhler G
  • Start Page

  • 459
  • End Page

  • 468
  • Volume

  • 19
  • Issue

  • 3