To investigate whether regulatory mechanisms of membrane TNF receptor as well as TNF receptor shedding could explain the enhanced sensitivity of memTNFΔ1–12 KI mice to intracellular bacterial infection, we analysed cells expressing TNFR1 and TNFR2 and total amounts of TNF receptors in mouse spleen before and after the infection. The gene discussed is TNFRSF1A; the disease is infection.