6533b837fe1ef96bd12a32e8
RESEARCH PRODUCT
An antigen-independent physiological activation pathway for L3T4+ T lymphocytes.
Tieno GermannHelga HuhnErwin RüdeFrank Zimmermannsubject
Antigens Differentiation T-LymphocyteT cellImmunologyReceptors Antigen T-CellMice Inbred StrainsGrowthBiologyMajor histocompatibility complexLymphocyte ActivationCell LineTosyl CompoundsMiceAntigenmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorAntigensReceptors ImmunologicAntigen-presenting cellMice Inbred BALB CHistocompatibility Antigens Class IICD28Receptors Interleukin-2T-Lymphocytes Helper-InducerCell biologymedicine.anatomical_structurePhenotypeImmunologyAntigens Surfacebiology.proteinInterleukin-2CD8Spleendescription
The data presented in this report describe an antigen-independent activation pathway leading to reinduction of proliferation of class II major histocompatibility complex (MHC)-restricted murine T cell lines that after previous antigen-specific stimulation reverted to a resting state. Antigen-independent proliferation and interleukin 2 (IL2)-receptor expression occur in the presence of splenic accessory cells, exogenous IL2 and a soluble factor(s) provisionally termed T cell-stimulating factor(s) (TSF). Each of these components is essential for inducing growth. TSF is found in the supernatant of an autoreactive T cell line upon stimulation with syngeneic accessory cells. Neither TSF nor accessory cells can be replaced by IL1 and by some other cytokines. Monoclonal antibodies against class II MHC molecules, the T cell receptor and L3T4 do not block this antigen-independent stimulation. This demonstrates that the function of the accessory cell in this system is not MHC restricted and that the T cell receptor is also not involved. Furthermore, it is suggested that the blocking of L3T4 molecules by antibody will mediate a negative signal only if T cells are triggered via their antigen receptors.
year | journal | country | edition | language |
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1987-06-01 | European journal of immunology |