week 6 + 7 (lymphatic) Flashcards
(38 cards)
1
Q
question: main role of lymphatic system? (connection to circ.)
A
- returning extra fluid that remains in tissue space
- puts it back into circ. system
- prevents fluid buildup
- also for immunity and disease resistance
**bc more fluid enters tissues than returns to blood through reabsorp.
2
Q
name: differences between lymphatic capillaries vs blood capillaries
A
lymph are:
- close at one end
- larger diameter
- thinner walls
⤷ bc no CT or musc. around it
- have flattened or irregular outline
⤷ bc valves
3
Q
question: primary vs secondary lymphoid tissues/organs?
A
- primary = site where lymphocytes are formed/mature
⤷ ex. RB marrow, thymus gland - secondary = site where lymphocytes are activated and cloned
⤷ ex. tonsils, appendix, spleen, lymph node
4
Q
define: lymphocyte
A
- primary cell of lymph. sys.
- allows body to resis infection and disease
5
Q
name: types of hemocytes (+define: hemocyte)
A
- hemocyte = cells that mediate immunity in invertebrate
⤷ insects - plasmatocytes = engulf the pathogens (phagocytosis)
⤷ majority of the hemocytes 95% - crystal cells = wound repair and engulgs microbes in hardened case + destroys them with peptides and prot.
- lamellocytes = rare in healthy insects, involved in encapsulation
⤷ prevents spread
6
Q
define: leukocyte
A
- cells involved in immune sys. of vertebrate
- WBC
- all nucleated
- in blood and interstitial fluid
- moves across capillary walls
- neutrophil, eosinophil, basophil, monocyte/macrophage, lymphocyte
7
Q
name + explain: types of leukocytes (5)
A
-
neutrophils
- phagocytosis to engulf damaged cells and foreign particles -
eosinophils
- deliver chemicals and enz. to kill parasites
- involved in allergic reactions -
basophils
- leaves circulatory sys. and accumulates at site of infection
- release chemicals to kill foreign particles
- involved in inflammation -
monocytes
- mature into macrophages
- engulf and destroy foreign particles -
lymphocytes
- B, T, natural killers
8
Q
name + explain: types of immunity (2)
A
-
innate (non-specific) immunity
- present at birth
- genetically determined
- resp. = not changed/specific based on danger (always same) -
acquired/adaptive (specific) immunity
- acquired when exposed to an antigen
- dep. on T and B cells
- 2 subtypes
a. active = antibodies dev. after exposure
⤷ nat. acquired = dev. after exposure to antigens in envrt.
⤷ artifically acquired = dev. after administration of antigen
b. passive = antibodies are transferred from another sources
⤷ nat. acquired = from transfer of maternal antibodies
⤷ artificially acquired = administration of antibodies
9
Q
name: types of physical barriers for immune sys.
A
- secretions
- hair
- stratified squamous epithelium
10
Q
question: how can there physical barriers work for immune sys.?
A
SECRETIONS
- wash away unwanted things
- destructive enz. and antibodies
⤷ kill pathogens
HAIR
- provides protection from hazardous materials and abrasion
STRATIFIED SQUAMOUS EPITHELIUM
- layers prevent things from going through skin into tissue
⤷ keratinized cells and desmosomes
- can also secrete enz. for degradation
- epi. cells = tight together
⤷ held by tight junctions
11
Q
name + explain: types of phagocytes (3)
A
-
neutrophils
- very common
- mobile
- fast acting
- in blood and tissues
- eat cell debris or bac. -
eosinophils
- less common
- eat foreign compounds and antibody coated pathogens -
macrophages
- emigrate from capillary to tissue spaces
- responds to chemokines (signaling prot.)
- 2 types
⤷ fixed = scattered in CT and immobile
⤷ free = can move around body
12
Q
explain: phagocytes (general job + how it does things)
A
- engulf foreign things
- 1st line of defense
- always attaches to target first
- either destroys the things itself or promotes it’s destruction
⤷ ex. activating other defenses - emigration/diapedesis
⤷ leaving capillaries by squeezing between endothelial cells
13
Q
explain: steps of NK cell to destroy a pathogen (4)
A
- recognition and adhesion
- recog. antigens and binds to pathogen - realignment of golgi
- golgi app. repositioned to be towards contact site w/ pathogen
- allows more efficient release of cytotoxic granules (ex. perforins) - secretion or perforins
- releases perforins when near antigens
- creates pores in mem. causing disintegration - lysis of abnormal cell
- cells bursts open and dies
14
Q
define: interferons
A
- chem. messengers that mediate coordination between other types of immune cells
- released by lymphocytes, macrophages, virus infected cells
- use paracrine comms (nearby cells, not through circ. sys.)
- 3 types
⤷ alpha, beta, gamma
15
Q
name + explain: types of interferons (3)
A
-
alpha
- prod. by cells infected w. viruses
- attracts and stim. NK cells
- enhances resistance to viral infection -
beta
- secreted by fibroblasts (synthesizes CT + connects and supports tissues)
- slows inflammation -
gamma
- secreted by T and NK cells
- stim. macrophages
16
Q
recap: name types of innate defense (7)
A
- physical barriers
- phagocytes
- immune surveillance (NK cells)
- interferons
- complement system
- inflammation
- fever
17
Q
explain: complement system in immune sys.
A
- coordinated action of prot. that help antibodies
⤷ enhances phagocytosis and inflammation - also helps lyse cells
18
Q
question: how does inflammation happen?
A
- localized, tissue-level resp.
- used to limit spread of infection
- starts w/ histamine and heparin release
⤷ by mast cells - increases blood flow and capillary permeability
- activates macrophages
⤷ attracted by chemokines - activates complement
- stim. clotting reaction
- increases regional temperature
- activates active defenses
**overall leads to red, hot, swelling in region of inflammation
19
Q
question: what is a fever? + what causes reaction?
A
- body temp over 37.2°C
- caused by pyrogens
⤷ fever inducing prot. - changes thermostat in hypothalamus to be higher
⤷ causes body T to increase to match new set point
20
Q
question: how can fevers be good? bad?
A
- inhibits some viruses and bac.
⤷ prevents spread + slows growth - increases metabolic speed
⤷ can increase tissue defenses and repair
**but too long fever -> becomes danger to normal cells
21
Q
name: properties of adaptive immunity (4)
A
- specificity
⤷ each T or B only resp. to specific antigen - versatility
⤷ many diff. types of lympho. (each fights diff. type of antigen) - memory
⤷ some active lympho. stay in circ. and can remember antigens - tolerance
⤷ immune sys. ignores “self” antigens
22
Q
question: where does each lymphocyte originate from?
A
- NK = red bone marrow
⤷ after exposure to interleukin-7 - B = red bone marrow
- mature T = thymus gland
⤷ from lymphoid stem cells that migration from red bone marrow to thymus
⤷ exposure to thymic hormones
**from RB marrow = hematopoiesis
23
Q
question: where does each lymphocyte migrate to after maturation?
A
- NK and B -> bloodstream -> peripheral tissues
- T -> bloodstream -> lymph nodes, spleen, lymphoid tissues
24
Q
question: how does chemotherapy impact immune sys. cells?
A
- chemo also attacks RB marrow
⤷ bc RB marrow is also fast-dividing - so chemo needs to be spaced out to keep immune sys. from lowering too much
25
explain: types of lymphocytes (3)
1. **T**
- helper T = secrete molecules to activate other lymphocytes
- killer T = secretes cytotoxic agents to kill invaders/dying cells
- adaptive imm.
⤷ need activation
- memory T
- cytotoxic T
2. **B**
- secretes antibodies
- produces antibody mediated immunity
- **NK**
- directly kill diseased cells
- innate imm.
⤷ no activation needed
- immunological surveillance
26
question: diff. between cell mediated and antibody mediated imm.?
- cell = cells themselves damage the pathogen
⤷ usually T cells
- antibody = bind to pathogen
⤷ releases antibodies to "prep" for other cells to kill it (ex. tagging, neutralize, marking)
⤷ usually B cells
27
explain: types of T cells (4)
**leukocytes -> lymphocytes -> T cells
**cytotoxic and memory prod. from same cell division
1. **cytotoxic** CD8+
- seek out and destroy infected cells
- body doesn't keep enough right away
⤷ needs few days after first exposure to reach effective lvls of conc.
⤷ need to prod. more of the needed cells
2. **memory**
- do not differentiate further during first exposure
- but if antigen comes again, memory -> cytotoxic
⤷ stays in reserve until needed
3. **regulatory/suppressor**
- suppresses resp. of other T and B cells
- limits degree of immune activation from a single stim.
- bc E expensive + can damage normal cells if full power
4. **helper** CD4+
- secretes cytokines
⤷ stim. T cell division (memory and cytotoxic)
⤷ enhances nonspecific defenses (ex. macrophages)
⤷ attracts cytotoxic T
⤷ promotes activation of B -> antibodies
28
question: memory B vs memory T cells?
- B prod. antibodies, T attacks
- similar = both stay in reserve until second exposure
29
explain: structure of an antibody
- 2 parallel pairs of polypep. chains
⤷ 1 heavy, 1 light
- 5 heavy chains determine type
30
name + explain: types of antibody classes (5) (only explain G and M)
1. **IgG**
- resistance against viruses, bac, toxins
2. **IgE**
3. **IgD**
4. **IgM**
- first class secreted after antigen exposure
⤷ non-specific
- IgG prod. accelerates -> IgM conc. increases
⤷ IgM = placeholder for IgG
5. **IgA**
31
name: examples of methods to eliminate antigens by antibodies
- neutralization
⤷ occupying binding sites to prevent from affect body
- stim. inflammation
- attracting phagocytes
- agglutination
32
explain: primary and secondary resp. to antigens
PRIMARY
- IgM starts
- IgG prod. starts later and rises higher than IgM
⤷ IgM decreases
- when IgG peaks = feeling better
**IgG delay is from time spent recog. the antigen
⤷ need to activate T cells (clonal expansion) to activate B cells to release antibodies
SECONDARY
- IgM and IgG both start together
- IgM still rises and falls around the same
- IgG increases much more
⤷ bc already recog. antigen so can skip to clonal expansion right away
**primary can be natural or artificial, secondary is natural
33
question: how are T cells activated? + how do they become memory T?
PRIMING
- antigen is first presented to T cell
⤷ induces EXPANSION for the first time
- after antigen lvls drop -> CONTRACTION
⤷ T cells die
- leftover T cells that don't die -> MEMORY T cells
⤷ still more #s than before infection
34
define: antigen presenting cells
- capture and process foreign antigens and display them on their surface using MHC
⤷ major histocompatibility complexes
- ex. dendritic cells, macrophages, B cells
- important for T cells to coordinate resp.
35
explain: MHC
- major histocompatibility complex proteins
- essentially tags for antigens
- bind to peptide frag. for T cells to see
- 2 classes
1. class I
⤷ on surface of all cells on body
⤷ puts on "self" tag to tell T cells not to attack
2. class II
⤷ on macrophages, B cells, dendritic cells
⤷ displays foreign tag for T cells to ID and attack
36
question: which parts of MHC and antigens do T cells recog.?
- alpha/beta dimer of T cells recog. peptide frag. on APCs
- helper T cells binds to MHC class II molecules
- cytotoxic cells bind to MHC class I
37
explain: maturation of T cells (both RB marrow and thymus)
- all T cells start from RB marrow
⤷ some migrate to thymus
THYMUS
- +ive selection in thymic cortex
⤷ must learn to recog. self-MHC to survive
- -ive selection in thymic medulla
⤷ if bind too strongly to self-antigens -> eliminated
RB MARROW
- diff. into CD4 (helper) or CD8 (cytotoxic)
38
question: how does herd immunity work?
- only works if majority are getting vaccinated
⤷ allows some of the community to stay unvax
- helps protect vulnerable members in a community
- large portion of community = immune -> hard to spread disease
