Introduction to the Immune System I and II Flashcards
1
Q
What are the general features of innate immunity?
A
- part of your immune system that you are born with
- exists before exposure to an antigen
- not improved by repeated exposure; no memory; not specific to any antigen
- physical components include skin, endothelium & epithelium, coughing, sneezing, crying, urination, and normal flora
- biochemical components include complement, lysozyme, pH, interferons
- cells include phagocytes (neutrophils, monocytes, macrohpages, dendritic cells), NK cells
2
Q
What are the general features of adaptive immunity?
A
- learned over time, through exposure to foreign substance
- specific for that antigen, enhanced by repeated exposure; does have immunological memory
- no physical components
- biochemical: antibodies, cytokines
- cells: B & T lymphocytes, dendritic cells
3
Q
What are the mechanisms of innate immunity?
A
- epithelial surfaces like skin and GI tract are PHYSICAL BARRIERS (tight junctions) that have antimicrobial properties (pH, flow of fluid, antibacterial peptides, motion of cilia)
- complement system involves plasma proteins that, when activated, can LYSE OR OPSONIZE PATHOGENS. It also acts as a chemical signal to trigger immune response to that area
- in the tissues and circulation, immune cells like macrophages, neutrophils, and dendritic cells KILL MICROBES and initiate an INFLAMMATORY RESPONSE
4
Q
What are the roles of complement components in the innate immune response?
A
- complement works to INDUCE INFLAMMATION, OPSONIZE OR LYSE PATHOGENS.
- It is a cascade that begins once a pathogen enters the body and is recognized by the complement
- activated complement can use CHEMOTAXIS to draw the attention of the rest of the immune system (attract macrophages and neutrophils)
- it can also coat the cell (opsonization) to make it more likely to be phagocytized
- finally, it can form a membrane attack complex (MAC) that will puncture the membrane of the pathogen, causing cell death
5
Q
How does the innate immune system recognize ‘self’?
A
- Pathogen-Associated Molecular Patterns (molecules found on nonself, ie bacteria) are recognized by Toll-like Receptors (TLRs) and NOD-like receptors (NLRs)
- TLRs recognize functional groups that are on the surface of the pathogen, such as peptidoglycan that is the cell wall of bacteria. Other examples are lipoproteins and lipopolysaccharides (LPS). TLRs can also recognize elements inside the cell, but they must do it in an endosome because they sit on the plasma membrane (membrane-bound sac inside the cytoplasm of the cell)
- NLRs recognize patterns within the cytosol of the cell. There are at least 23 genes of these in humans. They typically interact with microbial ligands inside the cell, activating the NLRs and producing signals that will enhance inflammation
- in complement system, complement proteins assemble a complex that punctures the cell membrane. In human cells, CD59 binds to the complex and prevents binding of C9, which forms the pore. Thus, complement cannot lyse human cells
- TLRs and NLRs (as well as other stimuli) induce the inflammatory response and activate cells, increasing the killing capacity of phagocyte, cytokines, and virus resistance
- interferons are secreted once the anti-viral system in most body cells detect an infection. Interferons can act on the same cell or neighboring cells. This will shut off protein synthesis and activating RNAse to digest RNA, effectively preventing the virus from replicating and infecting other cells
6
Q
What is the clonal selection model?
A
- at any time, body is filled with ‘clones’ of naive B and T cells, each with different antigenic specificities on their surface. (B cells have immunoglobulins, Ig, on their surface; T cells have T cell receptors, TCR)
- once an antigen binds to the antigenic specific receptors on a cell of the adaptive immune system (naive B or T cell), that cell with that specific Ab will replicate and produce many cells capable of producing that same Ab. These plasma cells then pump out the antibody in order to defeat the infection. (this is true for B cells). T cells will become activated and will develop either into helper or cytotoxic T cells
- some of these selected cells are set aside to remember the pathogen in case it is encountered in the future
7
Q
How is antigen receptor diversity generated for B and T cells?
A
- too many combinations for there to be a single gene for every known pathogen
- instead, there are many possible combinations of genes that can create the variable regions of antibody and T cell receptors. The variable region of the antibody or receptor is what recognizes the antigen.
- there are many genes for each segment. For a heave chain, a V segment, D segment, and J segment are randomly selected. The light chain is similarly assembled
- the genes rearrange during B cell formation. After development RNA splicing will remove extra genes
- the gene rearrangement, variable heavy and light chains make up for a huge amount of diversity in these antigenic receptors
- once a functional Ig is produced, the other loci is shut off (one of each chromosome). This ensures that the cell will only present one type of receptor, and produce one kind of antibody (maintain specificity)
8
Q
What are the effector functions of Helper T Cells (CD4+)?
A
- these cells help activate CD8+ T cell and B cells
- they secrete cytokines and activate dendritic cells
9
Q
What are the effector functions of Cytotoxic T Cells (CD8+)?
A
- these cells act in the killing of recognized pathogens (ie, virus-infected cells and tumor cells)
- they kill cells, not free-floating pathogens
10
Q
What are the effector functions of Regulatory T Cells (CD4+)?
A
- these cells help to control the immune response so that it does not run out of control
- they regulate the actions of the other immune cells, including T cells
11
Q
What are the four phases of the antibody response?
A
- lag phase
- exponential phase
- steady-state (plateau) phase
- declining phase
12
Q
What is the lag phase (first of the four phases of the antibody response)?
A
time between initial exposure and detection of antibodies (flat on graph)
13
Q
What is the exponential phase (second of the four phases of the antibody response)?
A
- increase of antibodies in the circulation
- occurs rapidly due to rising number of plasma cells (positive slope on graph)
14
Q
What is the steady-state phase (third of the four phases of the antibody response)?
A
rate of antibody synthesis equals the rate of degradation (graph is flat)
15
Q
What is the declining phase (last of the four phases of the antibody response)?
A
antibody synthesis is reduced as the immunogen is eliminated (slope declines)
