Publication | Closed Access

Analysis of A2a receptor-deficient mice reveals no significant compensatory increases in the expression of A2b, A1, and A3 adenosine receptors in lymphoid organs

Molecular PhysiologySignal TransductionAutoimmune DiseaseLymphoid OrgansImmunologyImmune RegulationReceptor (Biochemistry)Immunologic MechanismA2a Receptor-deficient MiceAutoimmunitySignificant Compensatory IncreasesMedicineCell BiologyCell Signaling