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Describe the capsular structure of a lymph node; what are the functions of the LN?

Capsule of lymph node is made up of type III collagen (made by reticulin fibers!), extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages, Antibody production (via activation), storage and activation of B and T cells via bringing antigens from lymph by APCs or alone

T/F a lymph node is a primary lymphoid organ.

false; secondary

Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex, paracortex, medulla and sinuses)?

The interstitial tissue of a lymph node is structured into the cortex on the outside which is densely cellular which transitions into the paracortex which is less dense and then the medulla which is least dense. The cells that inhabit these tissues are B cells (in both inactive and active follicles), T cells, and plasma cells respectively. The cells came from the lymph and vasculature. Afferent lymphatics pierce the capsular structure and empty into the subscapular sinuses which are continuous with the cortical sinuses which are then continuous with the paracortical sinuses and then the medullary sinuses. These sinuses are closely adjunct to the cords of the corresponding tissue and allow for interaction between lymph and the lymphocytes in the ln tissue and are lined with macrophages that engulf antigens and present them to the lymphocytes in the adjunct cords. The sinuses empty in the efferent lymphatics.

T/F the secondary follicles found in the cortex of a lymph node are densely colored.

False, secondary follicles have pale central germinal centers; primary follicles are dense

What are HEV? Where are they found? where does the vasculature of the lymph node travel to?

High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is how these lymphocytes get there in the first place!); They are found in the paracortical section of the LN; the vasculature travels through the entire ln, once lymph dont find an antigen to attack they empty back into veins or into efferent lymphatics

What happens in a secondary follicle?

isotype switching (activated by Th2 cell signals and cytokines), somatic hypermutation

What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?

An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and then follicular dendritic cells will select for plasma cell which will go to medulla and secrete Ab

What part of the lymph node specifically expands during a cellular immune response? when would this occur?

Paracortex; viral infection

what can cause a lymph node enlargement?

local infection/inflammation; infection of the ln itself; metastasis

What bugs can actually infect the lymph node itself?

Mycobacterium Tuberculosis, Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

What portion of the lymph node is not well developed in DiGeorge Syndrome?


what lymph node drains the upper limb?


what lymph node drains the breast?


what lymph node drains the stomach?


what lymph node drains the duodenum, jejunum?

Superior mesenteric

what lymph node drains the sigmoid colon?

inferior mesenteric

what lymph node drains the rectum (above the pectinate line)?

internal iliac

what lymph node drains the anal canal (below the pectinate line)?

superficial inguinal

what lymph node drains the scrotum?

superficial inguinal

what lymph node drains the testes?

para aortic

what lymph node drains the thigh?

superficial inguinal

what lymph node drains the lateral side of the dorsum of the foot?


what are the sinusoids of the spleen? what is the difference between a spleen and a lymph node?

the red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap antigens from local tissue but the spleen also does the same for the blood!

what type of fenestrations are found in the red pulp of the spleen?

barrel hoop basement membrane fenestrations

what is the white pulp of the spleen?

surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

what is the marginal zone of the spleen? what happens there?

found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrophages and those not eaten empty back into venous sinuses

what are the PALS?

periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp, contain T cells

what is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>

closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back into venous sinuses; all end up going through open circuit

other than eat and bite RBCs what else do Macrophages of spleen do>

remove encapsulated bacateria

what are four results of a splenectomy?

1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

what bacteria are a splenectomy patient most susceptible to? why?

N. meningitidis, H. influenzae, S. pneumonia, Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule

what are howell jolly bodies?

nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

what are target cells?

cells that stil have weird parts of their membrane that macrophages usually bite off

what is the thymus ? where is it located? is it encapsulated? how many lobes does it have?

the place of T cell diff and maturation; ant mediastinum above heart; yes; 2

T/F the thymus and its comp derived from 3rd branchial pouch

false- the lymphocytes are mesenchymal origin

how is the thymus organized? what happens in each section?

Into cortex and medulla; cortex is where immature T lymphocytes enter, at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs, reticulin cells and hassalls corpuscles are (dead reticular cells)

in thymic development, what is the positive selection? negative selections?

when you select for which MHC it will have; take out the lymphs that self react

are the MALT/GALT encapsulated?


which type of selection of thymic development provides central tolerance?

negative selection

what links the adaptive and innate immunity?

complement activation (active in both)

what kinds of receptors activate innate immunity?

TLR ad nuclear receptors

T/F RBCs have blood group antigens.


T/F RBCs have MHC class glycoproteins.


What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?

glycoproteins; HLA

Which HLA's are included in MHC I? MHC II?

A, B, C; all the D's

What are MHC's necessary for? By themselves?

T cell activation; no with CD 4 or CD 8

What is MHC I made out of? where is it found? What does it bind to? What type of antigens does it present?

an alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?

All MHC 1/CD8

What is MHC II made out of? where is it found? what does it bind to? What type of antigens does it present?

an alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

how is the antigen loaded onto a MHC II?

an acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain which is sitting in spot of antigen and stabilizing the MHC II

which MHC presents intracellular peptides? how so?

MHC I; from RER with help of the B2 microglobulin

which disease is associated with HLA A3?


which disease is associated with B27?

(PAIR) Psoriasis, Ankylosis Spondylitis, IBD, Reiters; all seronegative spondylopathies

Which disease is associated with B8?


which diseases are associated with DR2?

MS, hay fever, SLE, goodpastures

which disease is associated with DR3?

Diabetes mellitus (DM) type I

Which diseases are associated with DR4?

DM type I and rheumatoid arthritis (RA)

Which diseases are associated with DR5?

Pernicious Anemia and Hashimotos

which disease is associated with DR7?

Steroid responsive nephrotic syndrome

What are the three types of lymphocytes?

B, T, and NK cells

T/F all the lymphocytes are apart of the innate system.

False! only NK cells

What type of cells do NK cells attack? with what tools? by necrosis or apoptosis?

tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

which interleukin receptor is required for NK development? activation?

IL 12, interferon Beta and interferon alpha

what are the two signals to kill for NK cells?

lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

what prevents NK cells from killing normal cells if their default is to kill?

MHC class molecules bind to KIRS or CD94 to prevent killing

What are the major functions of Antibodies?

opsonize bacteria (for enhanced phagocytosis), neutralize viruses (igG), activate complement (igM and igG), sensitize mast cells (igE)

What are the function of B cells?

Make antibody, allergy type 1 (IgE), Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

What are the T cell functions?

CD4+ T cells help B cells make Ab, produce gamma interferon to activate Macrophages, CD8+ T cells kill viruses directly, delayed cell mediated hypersensitivity, acute and chronic rejection

Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response

Legionella, N. gonorrhea, L. monocytogenes, viruses, protozoa (leismaniasis)

T/F the T cell precursor in the BM has both CD 8 and CD4?

false- in the cortex of thymus

where do NK cells develop?

not thymus- BM

What are the three types of APCs?

Macrophages, Dendritic cells, B cells

T/F B cells do not require a second signal

False! B cell class switching requires a second signal

what are the two signals required for Th1 cells? what happens after then activated?

MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

What are the two signals required for T cells? what happens after?

MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

What are the two signals required for B cell class switching? which is the second signal?

CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4,5,6) from Th2 cell; CD40 is actually the second signal

Which helper T cells' development is induced by IL 4? IL 12?

Th2; Th1
(remember, IL4/Th2/CD40 ligand; IL12/Th1/IL2 receptor)

Which T helper cell activated Macrophages? by secreting what? what else does Th1 secrete? for what?

Th1; interferon gamma; IL 2 for cytotoxic T cell activation

How is Th1 helper cell inhibited?

cytokine IL 10 secreted by Th2

what do macrophages secrete that activate Th1 cells to secrete interferon gamma?

TNF alpha and IL1

T/F the Th2 regulate the cell mediated response.

False. Humoral

Which cytokines do Th2 release and for what?

IL 4,5,6 for B cell class switching, IL 10 to inhibit TH1

what secretes IL 4?

basophils! THey want IG E class switch!

which cytokine inhibits TH2 cells? secreted by who?

Interferon gamma; Th1

what does granzyme do? who secretes it?

its a serine protease that activates apoptosis; NK and CD8

what does granulysin do?

antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

what is the general structure of an Ab?

2 heavy chains and two light chains

T/F the two constant parts of the light chains of an antibody contribute to the Fc region

FALSE. only the heavy chains contribute to the Fc region

T/F the two heavy chains of an antibody contribute to the Fab portion


T/F the Fab (antigen binding) determines the isotype

false! idiotype; the Fc portion determines the isotype

To what portion of the Antibody do the complements bind?


T/F the Fc region is found on the N terminal

False; found on the carboxy terminal

what type of side chains are found on Fc region of an antibody?


So antibodies are the effectors for the humoral response. List some of their functions.

cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

Name 5 ways Antibody diversity is generated?

1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random addition of nucleotides at the end of the chains

where do somatic hypermutation and class switching occur?

in the germinal center of secondary follicles (In the paler center)

what do multimeric antibodies require for assembly?

A j chain

Which antibodies can be multimeric?

IgM and IgA

which antibodies can bind complement?

IgM and IgG

which antibodies prevent antigens from binding mucosal surfaces?


which antibody activate mast cells, basophils, and eosinophils?


what happens in order for class switching to occur (after being activated by IL and cd40 L)?

alternative splicing of mRNA

which is the main antibody in the delayed or secondary response to an antigen?


which is the most abundant antibody in blood?


can igG cross the placenta?


which is the main antibody that provides passive immunity to infants?


T/F IgG opsonizes.


T/F IgG can not neutralize.


T/F IgA fixes complement.


T/F IgA is a dimer in circulation.

False! Monomer in circulation, dimer when secreted

How does igA cross the epithelium?

by transcytosis

what is colostrum?

the igA found in breast milk

What does IgA pick up from epithelial cells before being secreted?

secretory component

which antibody is involved in the primary response or immediate response to an antigen?


T/F IgM can both fix complement and cross the placenta

false! can fix complement but cant cross placenta

T/F IgM is a monomer

False! IgM can exist as a pentamer also

What does it mean if there are igM in the serum at birth?

since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

what do mature naive B lymphocytes express?

IgM and IgD

T/F IgE has the lowest concentration in the serum


What does IgE do on the surface of the mast cell to induce inflammatory mediator release?

cross link

Which antibody mediates immunity to worms? how?

IgE; by activating eosinophils

If an antigen lacks a peptide component how does the adaptive immunity attack it? what type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?

This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues- IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then there is memory and igE attack is all we get; this is called Thymus independent antigens; Bugs that do this are bugs with lipopolysaccharide from envelope of gram negative or polysaccharide capsular antigen. Since spleen is where all igM are housed and produced, then there will be increased risk for infection by these types of organisms that lack a peptide component.

how do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?

give a vaccine with a peptide comp from it that the cell mediated immunity otherwise cant get to! like h.influenzae vaccine. then class switching and memory response can occur

what ensure that a memory response is generated?

if there is class switching and plasma cell production (that is when memory cells are produced)

what are complements in the complement system? what activates them? there seems to be different ones, what are these pathways called?

proteins; IgG, IgM, endotoxin (microbial surfaces in general- nonspecific ones also), mannose binding Lectin; classic, alternative, MB pathway (resp)

how does complement link innate and adaptive?

adaptive uses classic pathway to kill; innate uses alternative pathway to kill

What is the end result of complement activation? what bugs are this important for? through what pathway and why?

MAC (membrane attack complex) which is activated by C5b-C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia, H.influenzae, B perfussis for example) and other organisms with non peptide antigens because IgM coats these and through the classic pathway these can then be killed

what part of the complement system also acts as an opsonin? what is opsonization? can you name two other opsonins?

C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

T/F complements are acute phase reactants.


where are complements produced?

liver! (they are proteins circulating in the blood)

How does the alternative pathway lead to MAC activation?

soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation

T/F the alternative pathway is the only constutively active complement pathway


If the alternative pathway is constitively active, how come normal cells don't get attacked with MAC?

DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

after C3 spontaneously hydrolyzes to C3b and C3a, what happens to C3a?

its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

other than C3a, what other complement acts as an anaphyloxin?


Describe the Mannose Lectin pathway

some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway

describe the classic complement pathway.

IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

what are C1, C2, C3, C4 important for?

viral neutralization of igM and IgG!

what happens in a deficiency of C1 esterase inhibitor? DAF?

hereditary angioedema; PNH

What happens in a deficiency of C3?

severe recurrent pyogenic sinus and resp tract AND increased susceptibility to type III hypersensitivity like SLE

what happens in a deficiency of C5-C8? why dont you get recurrent pyogenic infections like in C3 def?

septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

what is hereditary angioedema? What are the C3 levels?

Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx

In order to produce Antibodies, does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).

no! That is why they are different from T cells- they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation, it then gets activated into a plasma cell! same for type II or III hypersensitivity except the antigen is usually harmless (like an RBC cell slight altered with penicillin on it).

explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.

for some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (entire immune system recognizes it as non self)

is IgM an opsonizer?


Name the three opsonins

CRP, C3b, IgM

name two endogenous pyrogens

IL 1 and IL 6

Name three things that IL 1 does as a cytokine. other than the liver, who secretes IL 1

induces fever, chemokine secretion to recruit, activates adhesion molecules; macrophages

Other than stimulating fever, what else does IL 6 do?

stimulate the liver to release acute phase reactants

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