ILCs
T/F: ILCs express clonally distributed diverse antigen receptors
False: They do not express clonally distributed TCRs
T/F: NKs express diverse, clonally distributed antigen receptors
False. They use germline DNA-encoded receptors
This pathway is triggered by mannose-binding lectin (MBL)
Lectin pathway
Adalimumab, etanercept, and infliximab are therapies for RA, PsA, AS, and IBD that target this cytokine
TNF
This ILC uses transcription factor GATA-3 for differentiation
ILC2
The effect functions of NK cells are to kill infected cells and produce this cytokine, which activates macrophages
IFN-g
C6, C7, C8, and C9 assemble into a membrane pore called this
Membrane attack complex
Tocilizumab is this cytokine receptor antagonist; this cytokine stimulates Th17 differentiation
ILC3s produce IL-22 and/or IL-17 and express RORgt, like these helper cells
Th17 cells
NK cells respond to these cytokines produced by macrophages
IL-12 and IL-15
The classical pathway starts with this plasma protein that detects antibodies bound to microbial surfaces
C1q
Complete LOF mutations in the gene for this cytokine or its receptors cause severe, treatment-refractory VEO-IBD
IL-10
These cytokines activate ILC1s to produce IFN-g for defense against viruses
IL-12 and IL-18
This activating receptor on NK cells is a low-affinity receptor for IgG (IgG1 and IgG3) and kills infected cells coated with antibodies via antibody-dependent cell-mediated cytotoxicity
CD16 (FcgRIIIA)
These cleavage products are also know as anaphylatoxins
C3a and C5a
Interferon-gamma
Lymphoid tissue-inducer (LTi) cells are a subtype of these ILCs and express lymphotoxin-a and TNF
ILC3s
The NKG2D receptor associates with this signaling subunit that stimulates NK cell cytotoxicity against target cells
DAP10
These 3 pentraxins can bind C1q and initiate the classical pathway
CRP, SAP, PTX3
Emapalumab is a monoclonal antibody that binds and neutralizes this cytokine for treatment of primary HLH and MAS
Interferon-gamma