Innate versus Adaptive Immune Response

Myeloid cells, such as granulocytes, monocytes, NK cells, DCs, contribute to the innate immune system in recognizing invading pathogens and tissue damage. These cells are activated upon contact with microbial and damage patterns (PAMPs, DAMPs) triggering a robust inflammatory response and release various pro-inflammatory mediators such as cytokines, interferons (IFNs) and specific cellular markers. This constitutes the immediate response to infection, provided by the innate immune system.

Adaptive immunity, which is required for the long-term, sustained response to infection, is activated through the classical MHCI and II/TCR interaction with activated dendritic cells. Interferons also act as a key link between the innate immune response and activation of the adaptive immune response.

Diagram showing the innate versus the adaptive immune response

CD64 (FCγ-RI)

  • Provide a first line of recognition and defense against infections
  • Bacterial infections, leads to release of type II IFN (IFNγ), which strongly induces the expression of CD64 on neutrophils.

CD169 (Siglec-1)

  • Adhesion receptor, recognizing sialylated glycoproteins and glycolipids of viral membranes
  • Viral infections, leads to release of type I IFNs (IFNα, β), which strongly induces expression of CD169 on monocytes


  • MHC-Class II receptor mainly involved in viral antigen presentation to T cells
  • HLA-DR on monocytes is induced immediately after infection, slowly declining with exhaustion.


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