Innate immune response Flashcards
How do erythrocytes contribute to the functioning of the immune system?
RBCs transport immune complexes (Ab-Ag) to the liver and spleen where they can activate the complement system. RBCs have a complement receptor. Liver and spleen have a high macrophage density; an antigen presenting cell. Immune complexes can then be destroyed by phagocytosis with activation of the IS through APCs. Platelets can also release cytokines
What are the two main types of dendritic cells and what are their common characteristics?
Interdigitating dendritic cells and follicular dendritic cells, both have long processes and provide a link between the innate and adaptive response
Describe the structure and function of follicular dendritic cells.
Follicular dendritic cells are located primarily in the germinal centres of secondary lymphoid tissues (lymph nodes, spleen and MALT) where the present unprocessed antigens, particularly to B cells. They do not express CD80 or CD88, nor do they express MHC II. They do however have an FcR and a complement receptor.
Are FCDs required for B cell presentation?
They are not essential but they enhance the efficiency of B cell activation.
IDCs or DCs function:
They are located widespread throughout the body and present processed antigens, particularly to T cells. They do express MHC-II, CD80 and CD86 on their cell surfaces. Perform antigen presenting of protein antigens through the cleavage of proteins into peptide chains which are then transported to the cell surface. MHC-II binds to TCR on the T helper cells, which can recognise peptide. CD4 on T helper cells help solidify the bindign of antigen peptide to TCR. This is an obligatory process for processed antigens to be presented to TCRs.
What is the default mode of NK cells?
To kill all cells
How do MHC-I prevent NK cytotoxicity?
MHC-I is present on surfaces of every nucleated cell and prevents NK cytotoxicity through binding to inhibitory receptor on the NK cell surface. NK cells also have an activating receptor.
How are cancerous or infected cells killed by NK cells?
They are destroyed by two methods i) they do not produce MHC-I and an activator molecule (transmembrane) binds to the activating receptor, signalling cytocide or ii) they overproduce an activating molecule which overrides the inhibition of cytotocixity mediated by the MHC-I.
What do cancerous/infected show a lack of?
MHC-I. “Missing self” describes a lack of MHC-I which can occur in tumours such as lymphoma, melanoma and infections such as adenovirus and cytomegalovirus.
How is NK cytotoxicity mediated?
perforin and granzyme injection into defunct cells.
What are the two main ways in which a NK cell can recognise a target cell?
Killer activating receptor-mediated cytotoxicity (no inhibitory signalling) or antibody dependent cellular cytotoxicity; an example of the innate and adaptive working together; all cells of the innate response can perform this; require a Fc receptor which recognises antibody and cytotoxic-molecule production capabilities. NK cells are most efficient at ADCC.
What are the molecules of the innate response?
Pathogen recognition receptors, acute phase proteins (C-reactive protein), cytokines, defensins, complement.
What do PRRs do?
They recognise pathogen associated molecular patterns (PAMPs) which can cause certain cytokines to be released in response to activation. Cytokines operate on the liver to increase the secretion of APPs
What do APPs do?
common response seen in infection, plasma concentration change is rapid (both increase and decrease) and are collectively invovled to defend against infection and tissue repair.
What happens when the liver is stimulated?
Stimulated by cytokines such as IL-6 and TNF, liver produces C3, C-reactive protein (activated complement system) and fibrinogen for coagulation.