2.5.10 infection process Flashcards
which has a greater SA, outer skin or mucosal surfaces?
mucosal
which are the encapsulated organs with both diffuse lymphatic tissue and lymphatic nodules?
Lymph nodes, thymus, spleen
describe discrete lymphatic tissue
- can be 2-3 cells, nodule, or germinal center
- can be nodular (has germinal centers) or non-nodular
-HIGH ratio of lymphocytes to other cells
describe Diffuse lymphatic tissue
- LOW ratio of lymphocytes to other cells
- in GI or upper respiratory
- 2 or 3 lymphocytes interacting with each other
what category do MALT, GALT and BALT fall into?
secondary lymphoid tissue
_____ are very diffuse and transient (come and go as infection does)
MALTs
what are examples of discrete lymphoid tissue? are they temporary or permanent?
GALTs and BALTS
Permanent
_____ allow liquids to remain inside and also carry agglutinated molecules away
Mucin molecules
the tonsils and adenoids form a ring of lymphoid tissues called _______ around the entrance of the gut and airway
Waldeyers ring
what does the GI tract consist of?
Commensals, s-IgA, Mucus
what are some of the things that commensal micro-organisms can do? (5)
- synthesize essential metabolites like Vitamin K
- break down plant fibers in food
- inactivate toxic substances in food or from pathogens
- prevent pathogens from benefitting from resources of human gut
- trigger immune response across epithelial border
In peyers patches, what cell brings in bacteria from gut lumen to GALTs?
M cell
Once antigens are brought into peyers patches, what happens?
dendritic cells and lymphocytes are waiting, B-cells and T-cells look for interactions so they can differentiate into effector T-cells or plasma cells
______ can extend processes across the epithelial later to capture antigen from the lumen of the gut
dendritic cells
Native lymphocytes that are activated in Peyers patch give rise to _____ that travel in the _____ and go out to the ________
- effector cells
- lymph/blood
- mucosal tisssue
what are cells found in mucosal tissue?
effector leulocytes, CD8, CD4, plasma cells, dendritic cells, mast cells, dendrites
do we want to produce inflammation in the bowel?
NO
from blood vessels, effector T-cells bind to intestinal vascular endothelium and enter the _________. Here the T- cells bind to _______
- lamina propria
- chemokines expressed by intestinal epithelium (CCL25)
s-IgA has multiple mechanisms and they are all _______
non-inflammatory
what are s-IgAs different mechanisms?
- export toxins and pathogens from lamina propria while being secreted
2.bind and neutralize antigens in endosomes - can bind and neutralize pathogens and toxins on gut surface
- secreted IgA can bind pathogen on M-cell and take it to lymphoid tissue
- Lymphoid IgA picks up antigen in endosomes and takes it to lymphoid tissue
____ has a long fold region that is subject to proteases, _____ has a short fold region that wont get proteased.
IgA1
IgA2
If there is a lack of ability to produce IgA, more what is produced?
IgM
Secretory _______ (2) protects mucosal surfaces from microbial invasion
IgM, IgA
IgG being transported from the blood —> lamina –> gut lumen by ______ is considered ______ (passive or active)
FcRn
- passive NOT active
what is an example of innate immunity on mucosal surface cells?
NOD2 proteins in cytosol of RBC
NOD2 proteins in cytosol of RBC respond to bacterial products by activating _______ ( just like TLRs)
NFkappaB
Bacteria are recognized by _______ on cell surface or intracellular vesicles, while _______ recognize bacteria entering the cytosol
TLR
NOD1, NOD2
what kind of response do we want against worms? why?
antibody, cellular response can damage the host
______ triggers protective antibody responses against worms while _____ triggers a harmful cellular response
TH2
TH1
the secondary response is ________ than primary response
stronger, more specific
the majority of T-cell and B-cells that are activated become _________, but the minority becomes ________
- short lived effector cells ( effector T and plasma )
- long lived memory cells
______ antibody amount increases with each infection. _____ antibody increases exponentially, while ______ affinity doesnt change much at all
IgG
IgG
IgM
In primary response _____ binds to pathogen and there is production of ______
-Naive B cell
-low affinity IgM antibodies
In secondary response _____ binds to pathogen coated with antibody and there is production of ______
- naive b cell (activation prevented) and Memory B cell
- production of high affinity IgG, IgA, IgE
what is an example of how memory response can be detrimental?
If a Rh- mother carries an Rh+ fetus, then becomes pregnant with another RH+ fetus
how can B-cell memory response be evaded?
antigen changes epitopes
_____ remains around longer than an antibody molecule
T-cell memory
_______ affects memory surface markers
mRNA splicing
how do you recognize a naive CD4 T cell?
it has CD45RA that has ABC in gene transcript
how do you recognize a memory/effector CD4 T cell?
it has CD45RO that excludes ABC (have been spliced out)
when memory cells are directly activated from naive T-cells _____ turns into ______. these cells go on to be _____ & _____
CD45RA –> CD45RO
-central memory cells that express CCR7 and effector memory cells that LACK CCR7
where do central memory cells with CCR7 go?
remin in lymphoid tissue
where do effector memory cells without CCR7 go?
migrate to tissues
some effector cells become _______ and most effector cells ____
-quiescent memory cells
-die after a few days
where are gamma/delta T-cells located?
near epithelial tissue
____ are MHC class 1-like molecules that bind gamma/delta receptors and induce infected cell to die from apoptosis
MICs
how do MIC and NK cells work together to kill infected cells?
- MHC1 + NK cell = no killing of cell
-MIC + NK cell = killing of cell
