Crohn’s disease belongs to organ - specific autoimmune diseases. Yet still unknown microbial or environmental antigens start complex autoimmune processes resulting in an intestine wall damage. T - cells (TH1) play a principle role in immunopathological reactions, esp. in their initial phases. Crohn’s disease is genetically determined; out of many genes involved, the NOD - 2 is of paramount importance. NOD - 2 encodes an intracellular pattern recognition receptor (PRR) that inhibits intracellular signalling induced by TLR - 2 ligation by peptidoglycan present in the cell wall of many bacteria. Its insufficient activity, caused by the NOD - 2 mutation frequently observed in the Crohn’s disease patients, leads to uncontrolled inflammatory processes. They are further supported by an enhanced activity of the transcription factor Smad - 7 what results in insufficient immunosuppressive activity of TGF - β. Understanding of the Crohn’s disease immunopathogenesis has enabled a biological therapy by monoclonal antibodies against the proinflammatory cytokine TNF (infliximab) and the α4β1 - integrin (natalizumab), respectively.