10/29 immunology Flashcards

1
Q

A peripheral lymphatic organ that filters the blood, rather than the lymph!

A

Spleen

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2
Q

How is the spleen analagous to the lymph nodes?

A

It can trap antigens and pathogens present in the blood and promotes immune responses as happens in lymph nodes.

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3
Q

The culling funciton of the spleen

A

it can turnover old blood cells

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4
Q

The organization of the spleen

A

thick capsule with irregular extensions into the organ called trabeculae

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5
Q

The divisions of the spleen

A

red pulp; Whit pulp; marginal zones

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6
Q

The structure of Red pulp in the spleen

A

contains large sinusoids and CT aggregates called cords

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7
Q

function of the red pulp in the spleen

A

involved in blood cell turnover and antigen trapping

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8
Q

Structure of the white pulp

A

aggregations of lymphocytes surrounding central arteries

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9
Q

the function of white pulp

A

involved in immune responses.

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10
Q

boundry between the with and red pulp

A

marginal zones.

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11
Q

What is the orginization of blood flow in the spleen

A

blood in in trabecular artery: come in CA central artery (between red pulp and white pulp) surrounded by Periarterial lymphatic sheath (PALS, which are T-cells). Then penicillar arteriole that go to open circulation or closed circulation and to the sinus and out trabecular veins

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12
Q

what is a peripheral immune organ as apposed to a central one

A

where imune cells act as apposed to where they are “educated”

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13
Q

what is the “white pulp” in reference to the blood flow?

A

it is the PALS or T-cell sheath that is around the central arteries.

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14
Q

what is open circulation?

A

the edge of the white pulp, the morginal zone, blood is dumped directly into the rred pulp tissue. blood cells must push through the CT and return to the circulation by entering sinusoidal cappillaries from the outside!

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15
Q

as we age how does the splenic blood flow change

A

As an antigen is trapped and B-cell response happens then you gen a group of lymphocytes grow away from the central artery and make it not so central any more (this is called a germinal center) So the germ centers grow and shrink and appear and disapear so a new born wouldn’t have any

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16
Q

closed circulation:

A

penicillar arterioles merge with capillaries that carry the blood to the sinusoids

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17
Q

What is the histological appearence of the white pulp

A

not always “whiter” it is around a central artery, and will be a white or red flush around the central artery

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18
Q

Remove entire old cells.

A

Culling

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19
Q

how do we Pitting of RBC

A

macrophages can engulf nuclear fragments or parasites, leaving the rest of the cell intact

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20
Q

how complete culling

A

macrophages engulf old RBCs and destroy them

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21
Q

how are antigens presented in the spleen

A

antigen in blood trapped by APCs in marginal zone and presented to lymphocytes

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22
Q

what are the steps of immune activity in the spleen for blood borne antigens

A

Present antigens; B-Cell activate; peripheral response

23
Q

what is the CT in the red pulp

A

chords

24
Q

how do get B-cell activate in spleen

A

Cells get antigen and cells respond, begin clonal expansion making central artery eccentric

25
Q

how peripheral response from the spleen immun system that is

A

plams cells found in red pulp etc.

26
Q

how is T cell expansion different then B cells in the spleen

A

T cell expansion is more uniform

27
Q

what are the lymphatic tissue of the gut?

A

MALT, mucosal associated lymphatic tissue, airways, the urinary system…

28
Q

what can we see in all kinds of tissue slides now that we have studied the immune system

A

you’ll likely see germinal centers in tonsils and peyer’s patches and now you’ll know what they are

29
Q

what gender differences of the immune system are there?

A

women have more robust immune higher circulating Ig, fewer viral infections but also more autoimune though some are more common in men.

30
Q

What is a very large lymphocytes in the blood

A

they are natural killer cells (NK cells)

31
Q

what do NK cells do

A

they are good at kill invading pathogens and alter host cells.

32
Q

what is the derivation of the NK cells

A

they are derived from the uncommited lymphoid progenitor cell.

33
Q

how are NK cells different from other lyphocytes?

A

they have a fixed set of antigen receptors and are considered innate elements (they don’t examin antigens to activate)

34
Q

How can NK cells get around a virus that affects MHC expression?

A

they don’t use MHC to recognize and attack an infected cell.

35
Q

what do NK recognize?

A

they recognize virally transformed cells, IgG opsonization: They recognize infected cells that express stress proteins even if MHC is present

36
Q

what does the host MHC molecule receptor in NK cells do?

A

inactivate the NK cells

37
Q

what is the healthy vs. infected cell signal to NK cell

A

healthy has MHC class I receptor to inhibit NK and infected has stress proteins to activate the NK cells.

38
Q

How do you get the range of antigen receptors that are possible?

A

recombination-activation genes (RAG) will choose some region of Variable regions and then add some extra sequences of nucleotides and then take some of the genome and toss out and then get a random sequence for the production of the receptor

39
Q

how is the education of B and T cells different?

A

B cells: Negative selection only (kill B cells with receptors that see self antigens) T cells: Positive (allow cells to live if the TCR sees MHC, otherwise die) AND Negative selection (Kill T cells with receptors that see self-antigens)

40
Q

what would happen if you were born without RAG proteins?

A

severe combined immunodifficiencies becasue of no T or B cells

41
Q

what if immune cells go out to the periphery and don’t ever see antigens?

A

become inactive (anergy)

42
Q

what are thymus-independent antigens?

A

they are antigens that can be bound to sIg internalize, processed, and displayed on MHC class 2 and some antigen can then stimulate B cell response at this point without involvement of T cells. IgM is secreted but often for a limited time only

43
Q

what is the normal (thymus dependent) route of stimulating B cells?

A

Antigen bind to sIg, internalize, process, shown on MHC class 2 for first signal to B-cells. B-cell express CD40, Th cell forms cognate pair with B cell and its TCR sees an antigen peptide with high affinity, it expresses CD40L, a membrane boound cytokine that binds CD40. that, plus a release and binding of cytokines provide the second activation signal. “two handshake mode”

44
Q

Summary of adaptive immune system activation (B-cells)

A

Dendritic cell present to Th and B cells, (the Th cell have the CD28/B7 handshake to activate). then the Th cell will interact with the B cell that has already seen the same antigen (first B-cell handshake with antigen) and interacts with the CD40L/CD40 handshake (second handshake) and fully activate the B cell.

45
Q

IgM

A

first secreted; but will switch if there is more infection

46
Q

IgA

A

secreted across mucosal membrane of gut tears airway etc.

47
Q

IgG

A

abundant and soluble

48
Q

IgE

A

on mast cells and basophils to recognize infection!

49
Q

where do we further mutate and get better and better anti-bodies from the B-cells?

A

Germinal centers, isotype switching !!

50
Q

benefit of additional mutations and isotype switching

A

IgM is first antibody made against infecting pathogen: then somatic hypermution seletc for antibodies that bind more tightly to the pathogen; then swithching antibody isotype to igG allows dilivery of the pathogen to phagocytes.

51
Q

how do babies get immune system and how does it change after birth?

A

maternal Ig molecules from the mother through the placenta that persist for about six months. They make IgM at first and then at six month to year they start build up thier own immune system.

52
Q

How do we get IgA protection in the gut?

A

IgA secreting cell in the lamina propria gives IgA and that is given to the basal side of epithelium and that is receptor mediated mediated endocytosis, and transported to apical face, and receptor cleaved and IgA is bound to mucus!

53
Q

Mast cells use AB but how?

A

mast cells take IgE and bind to the surface of themselves and then the IgE on the surface bind bacteria and cause the cell to release histamine very quickly! this is a rapid response that can be associated with allergies.