Inhibitory receptors on NK cells possess proteolytic activity

Inhibitory receptors on NK cells belong to the ROS family

Inhibitory receptors on NK cells are TLRs

Inhibitory receptors on NK cells interact with MHC molecules

Inhibitory receptors on NK cells contain ITAM motifs in their cytoplasmic tails

Stimulates inflammation and fever

D) Triggers apoptosis exclusively in damaged cells

Triggers apoptosis exclusively in damaged cells

Binds to antigen sites, akin to antibodies

Reduces localized body temperature

The uptake of external proteases from the extracellular space occurs during signal transduction

Src-family kinases are not involved in signal transduction in B cells

Activates downstream signaling pathways, including the early phosphorylation of tyrosine residues on the ITAMs of Ig𝛼 and Ig𝛽 by Src 

Perforin is released during signal transduction

NF-κB is primarily responsible for phosphorylating the ITAMs

Non-neutralizing antibodies do not bind to antigens

Non-neutralizing antibodies participate in antigen processing

Non-neutralizing antibodies lack a variable region (Fab) necessary for antigen binding

Non-neutralizing antibodies are produced by B cells and neutrophils

Non-neutralizing antibodies can potentially worsen infections by causing antibody-dependent enhancement (ADE)

IFN-γ secreted by Th1 cells induces the upregulation of MHC II on the NK cell surface, allowing the NK cell to present endogenous viral antigens directly to naive CD4+ T cells

The NK cell's CD94:NKG2A heterodimer binds to HLA-E on a healthy cell, which sends a potent phosphorylation signal through ITAM motifs to activate the NK cell's lytic machinery

An NK cell identifies a tumor cell coated in IgG antibodies and binds to them using its CD16 (FcγRIII) receptor, initiating antibody-dependent cellular cytotoxicity (ADCC) 

A virally infected cell downregulates MHC I expression to evade CD8+ T cells; the absence of MHC I prevents the engagement of NK cell KIR (killer-cell Immunoglobulin-like receptors), removing inhibitory brakes and triggering degranulation

An NK cell recognizes MICA/B proteins on a stressed cell surface via its NKG2D receptor, which overrides inhibitory signals from MHC I molecules, leading to the release of perforins

Neutrophils can proliferate at inflammatory sites, but macrophages are terminally differentiated and do not have the ability to proliferate

Neutrophils express the high-affinity FcγRI receptor, which binds a specific opsonin attached to microbes and aids in phagocytosis, unlike macrophages

Neutrophils can survive for several days at sites of inflammation, whereas macrophages have a much shorter lifespan, lasting only hours

Both neutrophils and macrophages do not express MHC I

Both neutrophils and macrophages are capable of phagocytosis and can eliminate internalized microbes

Neutrophils

NK cells

T cells

B cells

ILCs

TLRs are only found on cells of the innate immune system

TLRs are crucial in antigen processing and presentation of antigens in DCs

TLRs recognize common molecular motifs, such as lipopolysaccharides, found on many pathogens

TLR genes undergo genetic recombination to produce a diverse range of highly specific molecules

TLRs are found only on the cell surface of T cells

The migration of mature, naive B cells to the site of infection is driven by TGF-β

Not B cells; rather, effector T cells migrate to the bone marrow

Mature, naïve B cells express CCR7, which binds to CCL19 and CCL21 to facilitate their homing to the lymph node

Plasmablasts, which are precursors of plasma cells, are only resident in the lung

Only immature, activated B cells migrate to the lymph node

B cell

Macrophage

Neutrophil

T reg cell

Innate lymphoid cell