Tolerance to viral antigens in Mov-13 mice carrying endogenized moloney-murine leukemia virus

Ronchese, Franca; D’Andrea, Emma; Collavo, Dino; Rossi, Anita De; Zanovello, Paola; Chieco‐Bianchi, Luigi

doi:10.1016/0008-8749(84)90317-4

Cited by 6 publications

(1 citation statement)

References 26 publications

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“…The data presented here do not allow us to define the mechanism operative in this system . However, by determining the frequency of precursors to GMuLV specific CD4+ T cells, as well as studying the effects of adoptive transfer of cells from neonatally treated mice on the immune competence of normal recipient mice, it will be possible to elucidate the events leading to the T cell nonresponsiveness seen after neonatal exposure to GMuLV Although our data agree with the results ofothers regarding the induction of neonatally induced nonresponsiveness to retroviruses (10,40,41), other systems have been described in which neonatal or congenital exposure to virus does not alter virus-specific immune responsiveness. The most notable example is LCMV Oldstone and colleagues (reviewed in reference 21) have shown that mice persistently infected with LCMV from birth produce similar amounts of antibody with the same specificities to that found in normal LCMV immune mice.…”

Section: Immunologic Nonresponsiveness To Murine Retrovirusessupporting

confidence: 86%

Neonatal exposure to thymotropic gross murine leukemia virus induces virus-specific immunologic nonresponsiveness.

Korostoff

Nakada

Faas

et al. 1990

The Journal of Experimental Medicine

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SummaryNeonatal exposure to Gross murine leukemia virus results in a profound inhibition of the virusspecific T and B cell responses of adult animals. Animals exposed to virus as neonates exhibit a marked depression in virus-specific T cell function as measured by the virtual absence of in vivo delayed type hypersensitivity responses and in vitro proliferative responses to virally infected stimulator cells. Further, serum obtained from neonatally treated mice failed to either immunoprecipitate viral proteins or neutralize virus in an in vitro plaque assay, suggesting the concurrent induction of a state of B cell hyporesponsiveness . The specificity of this effect at the levels of both T and B cells was demonstrated by the ability ofneonatally treated mice to respond normally after adult challenge with either irrelevant reovirus or influenza virus. The replication of Gross virus within both stromal and lymphocytic compartments of the neonatal thymus suggests that thymic education plays a key role in the induction ofimmunologic nonresponsiveness to viruses. mmunologic nonresponsiveness to autologous molecules and a variety of exogenous antigens can be linked to their presence during neonatal maturation (1-4). The consequences of neonatal exposure to viruses are considerably more variable (5, 6). Mice infected either neonatally or congenitally with lymphocytic choriomeningitis virus (LCMV)' or endogenous ecotropic retroviruses mount potent Ig responses and produce functional CTL precursors (7-9) . However, several recent studies have shown that exposure of neonatal mice to Moloney murine leukemia virus significantly reduced the frequency ofMoloney virus-specific CTL precursors and Ig levels (6, 10) . These contrasting results raise important questions concerning the ability of different viruses to induce tolerance, and the contributions of T and B cell components to virus-specific tolerance . To address these questions, the immune response ofmice exposed as neonates to NB-tropic Gross murine leukemia virus (GMuLV) was investigated . Exposure of neonates to GMuLV induces a state ofimmunologic nonresponsiveness that may be linked to intrathymic replication of this retrovirus .1 Abbreviations used in this paper: DTH, delayed-type hypersensitivity; GMuLV, Gross murine leukemia virus ; HAU, hemagglutinating units; LCMV, lymphocytic choriomeningitis virus; PFU, plaque-forming units ; RT, reverse transcriptase.Intraperitoneal injection of neonatal mice with GMuLV leads to the development of lymphatic leukemias typified by the presence of thymic lymphomas, and to a unique form ofpersistent infection within the central nervous system white matter (11-13) . The data reported here demonstrate that neonatal exposure to these murine retroviruses also induced a state of virus-specific T cell nonresponsiveness, characterized by impaired delayed type hypersensitivity and in vitro proliferative responses. Concomitant with this T cell defect was the functional inactivation of virus-specific B cells, as evidenced by the absence ofbot...

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Section: Immunologic Nonresponsiveness To Murine Retrovirusessupporting

confidence: 86%