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Immunity > T-Cells: Development and Activation > Flashcards

T-Cells: Development and Activation Flashcards

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1
Q

Danger Theory: The immune system protects the body from what three types of danger? (danger signals)

A
  1. Pathogens (Bacteria, viruses, fungi, parasites)
  2. Unusual tissue growth
  3. Damaged cells and tissues (housekeeping ability)

Danger signals can be given out by distressed cells and bacteria
Ex. Heat Shock Proteins
Ex. Uric acid is produced by damaged cells; signals immune system

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2
Q

Three functions of T lymphocytes

A
  1. Production of cytokines
  2. Cytotoxicity (kill other cells)
  3. Control of other immune cells
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3
Q

Major role of B lymphocytes

A

Production of antibodies by plasma cells

Plasma cells are a stage of B lymphocytes that are able to produce antibodies

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4
Q

Primary and Secondary Immune Responses (and tissue grafts)

A

If you stimulate with A a second time, the response will be much greater

If you give tissue graft to a patient and it rejects it the first time, the rejection to the same type of tissue graft will be even stronger the second time

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5
Q

Two major subgroups of T cells

A

CD4+ (TH):
Helper cells, get immune system going and direct it

CD8+ (Tc):
Cytotoxic (killing) ability

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6
Q

Th1-cell mediated immunity (CMI)

[CD4+, TH]

A

Produce IFNg and TNFa (Type IV Hypersensitivity)

Respond to intracellular pathogens

Steer the immune system; important in response to intracellular pathogens and viruses (listeria or TB)

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7
Q

Th2-Humoral Immunity

[CD4+, TH]

A

Produce IL-4, IL-5, IL-13 (Type I Hypersensitivity)

Controls antibody production

Helminths (parasitic worms), allergic reactions, extracellular pathogens

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8
Q

Th17

[CD4+, TH]

A

Produce IL-17 cytokine

Acts upon a number of cell types

Important in defense against extracellular bacteria and fungi
(Candida albicans)

Also play a role in defense against TB, but much less critical/well-defined

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9
Q

TReg

[CD4+, TH]

A

Can suppress (inhibit) the effector functions of CD4+ and CD8+ T cells.

AKA downregulate the immune response

TReg cells account for 5-10% of the CD4+ cells and express:
CD25 (part of cytokine receptor)
FOXP3 (surface molecule you can detect upon TReg)

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10
Q

Cross-regulation of Th1/Th2

A 
Th1 produces IFNa, IFNg
IFNa, IFNg inhibit Th2
IFNa, IFNg lead to macrophage activation
IFNa, IFNg induce more Th1
Activated macrophages release IL-12
IL-12 induce more Th1

Th2 produce IL-3, IL-4, IL-5
IL-3 promote Mast Cell growth (induce allergic responses)
IL-4, IL-5 induce B cell activation, which produce antibodies
IL-3, IL-4, IL-5 induce more Th2
IL-3, IL-4, IL-5 inhibit Th1

In certain responses, either Th1 or Th2 is usually dominant

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11
Q

Tc (Activation, 2 pathways)

A

Tc is activated by Th1 cytokines

Killing requires direct contact and conjugate formation

Pathway 1: Cytoplasmic granules = perforin + granzymes&raquo_space; apoptosis (via granzymes)

Pathway 2: Fas-Fas ligand interactions&raquo_space; apoptosis

Similar cytotoxicity mechanisms to NK and NKT cells

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12
Q

Antigen Presenting Cells (APC)

A

Types:
B cells, macrophages, dendritic cells

Can enzymatically process antigen

Present digested fragments to Th cells (that then stimulate Th cells)

Do this via MHCII molecules

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13
Q

B and T cells with antigen presentation

A

B cells can interact with antigens in isolation

T cells must have antigens presented to them (via APC)

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14
Q

Epitope

A

The part of the antigen (small part) that is recognized by the lymphocyte receptor

Antigenic determinant

T and B cells recognize different types of epitopes (usually)

For any antigen that contain many epitopes, some will be more presented more than others (immunodominant)

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15
Q

MHC I

A

Found on all nucleated cells

Present antigen to CD8+ (Tc)

Saying “kill me”

HLA-A, HLA-B, HLA-C

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16
Q

MHC II

A

Found only on APC

Presents antigen to CD4+ (Th) cells

Stimulating an immune response

HLA-DP, HLA-DQ, HLA-DR

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17
Q

Chains of MHCI and type of antigen it presents

A

Consists of:

  1. Polymorphic heavy (a chain): highly variable among individuals
  2. Non-polymorphic (constant) light chain (B-2 microglobulin): Essential for expression of MHCI, but not attached to MHCI heavy chain or the cell surface; not encoded within the MHC

Presents:
Endogenous antigen (formed inside the host cell)
Viruses, tumors
(Viral: takes over cell’s ability to produce proteins; viral antigens produced as if they are the cells own proteins)

Presents to CD8+ Tc cells

Can be increased by: IFNa,b,g

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18
Q

Chains of MHCII and type of antigen it presents

A

Consists of:
Polymorphic a and B chains (both encoded within MHC)

Found on specialized APCs (dendritic, macrophage, B cells)

Presents:
Exogenous antigen (originate outside of APC; ex. fragments of bacteria, viruses caught between cells, vaccines)

Presents only to CD4+ Th cells

Can be increased by: IFNg, a

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19
Q

Clonal selection (Process and Cell types)

A

All T and B cells have receptors for antigens

Genes are randomly changed around to get unique receptors that recognize antigens (somatic recombination)

Transposons “jumping genes”; gene segments detach, move up chromosome and reattach later on

T cells develop and produce millions of antigen receptors

The one that fits the antigen will undergo a change, receive a stimulus that activates it

The ones that don’t recognize antigens will fade away and die

The cell that by chance is specific for that antigen, you now get thousands of cells specific for that antigen (why your response is much greater the second time)

Cell types:
mostly Effector cells: T cells and plasma cells for B cells
Memory cells: Stay in lymph nodes; could be re-stimulated at later date

Via mitosis: identical parent and daughter cells

If this is not regulated, eventually you will end up with a tumor

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20
Q

Primary, Secondary, and Tertiary Lymphoid Tissue

A

1: Thymus (T) and Bone marrow (B)
2: Lymph nodes and tissues
3: Remaining areas where lymphoid cells are found

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21
Q

Which MHC molecules are found on macrophages?

A

Both
MHC1: Macrophage is a nucleated cell
MHC2: Macrophage is an APC

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22
Q

Thymus (what do T cells come in contact with? what develops on T cells? DN, DP, SP)

A

Bilobed organ lying over the heart (Sail shaped)

Contains many T lymphocytes at various stages of development

Committed T cells pass through the thymus where they undergo a selection process

Also contains thymic epithelial cells which express MHC molecules
These MHC molecules contain our own antigen; we do not want T cells to respond to this

In thymus:

  1. TCR develops
  2. Surface molecules change
  3. And CD3, CD4, CD8 (associated with TCR)

DN: CD3+ but DN for CD4+ and CD8+
DP: CD3+ and DP for CD4+ and CD8+
SP: CD3+ and either CD4+ or CD8+ (SP ratio ~2:1)
Once either 4 or 8, it’ll interact with MHCI or II and then develop

CBC w/ diff would be essential to elucidate the total lymphocyte count

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23
Q

Bone Marrow

A

Site of lymphocyte origin

T and B cells being existence here

T cells leave underdeveloped for the thymus

B cells mature and undergo type of selection to remove potential autoreactive cells

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24
Q

Movement through the lymphoid system

A
  1. Lymph moved along the vessels by contraction of the body’s muscles in a ONE-WAY system
    > Lack of effective muscle contraction can cause this movement to cease
    » Causes edema in the tissues (elephantiasis)
  2. Foreign antigens which enter the connective tissue are carried by the lymphatics to the nearest lymph node (draining lymph node)
    > You can get an enlarged lymph node from an infection (draining LN); it’s not carrying out all the activity required to get rid of that antigen
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25
Chronic Wuchereria Bancrofti Infection
After many years of infection | Microfilaria block lymphatic vessels, resulting in edema in legs, scrotum, and breasts
26
Lymph Node (APCs, 3 parts, blood supply)
Direct entity with own blood supply and own lymphatic vessels going out Where antigen presentation takes place Cortex: B cells in germinal centers (follicles- collection of cells) Paracortex: Mainly Th cells Medulla: Plasma cells Macrophages and dendritic cells found in cortex and paracortex (outer regions) Lymph, fluid that drains through these tissues, holds APCs that sample microbes circulating Dendritic cells pick up the microbes and transfer them to lymph nodes concentrating them there for immune activation
27
B cells > Plasma cells
When B cells form plasma cells, they go to the bone marrow and medulla in lymph node and start secreting the antibody They don't need to be at the site of infection because antibodies can move around through the blood stream
28
Spleen
Largest of the lymphoid organs, but not connected to the rest of the lymphoid system Hilum where the splenic artery and vein leave No lymphatic vessels supplying the organ Significant role in blood-borne diseases (malaria, capsulated bacteria) Also site of removal of damaged RBCs and platelets Filters blood capturing microbial antigens that have been concentrated by dendritic and macrophages Abundant phagocytes (destroy blood microbes) B cells located in follicles and white pulp of the spleen
29
Other lymphoid tissues
(Spleen, Thymus) Appendix Tonsils Adenoids Peyer's patches
30
GALT
Gut associated lymphoid tissue Peyer's patches Appendix GALT+BALT = MALT Mucosal-associated lymphoid tissue
31
BALT
Bronchial associated lymphoid tissue Respiratory tract lymphoid tissue GALT+BALT = MALT Mucosal-associated lymphoid tissue
32
How are antigens transported from mucosal surfaces to the lymphoid system?
M cells: Microfold Membranous cells
33
Lymphocyte Recirculation
1. Lymphocytes leave the blood circulation and enter the lymphatic system at lymph nodes 2. They leave the venous system through specialized epithelial cells HEV: High endothelial venules By diapedesis or extravasation 3. Re-enter venous circulation via thoracic duct Which enters the left subclavian vein
34
Langerhans cells
Type of dendritic cell of cutaneous surface (skin) Capture antigen which penetrates the skin and carry to draining lymph node where they process and present the antigens to T cells in the paracortex
35
TCRgd cells
Intraepidermal lymphocytes that are thought to be a first response to infection
36
Definition of Antigen
Used to be: molecules that induced antibody responses Now: any molecule that is recognized by BCR or TCR Can be large and the portion of the antigen bound by receptor is called the epitope
37
Haptens
NOT antigens Small molecules that by themselves cannot induce an immune response They are antigens but are not immunogenic They induce an immune response when attached to a larger protein (often host's own protein) Ex. nickel, penicillin, urushiol (poison ivy)
38
Adjuvant
Most isolated antigens require this to induce an immune response Third party compounds or substances which stimulate the immune system There are several in common use and their mode of action varies from type to type 1. Non-specifically stimulate lymphocytes 2. Prolong antigen persistence 3. Induce receptors on accessory cells
39
T Cell Epitopes
1. Much better defined than B cell epitopes 2. Usually between 8-11 AA for presentation by MHC I 3. Somewhere between 13-17 AA for MHC II * We don't have as many MHC types as we do T cell receptors* Must interact with MHC and T cell receptor at the same time AA comprising the epitope must be sequential T cell receptor is precise, MHC is broad
40
CD40L (ligand)
T cell surface molecule Interacts with CD40 on APC ``` Important for antibody class switching Lack leads to Hyper IgM syndrome (these patients lack CD40 and can't switch antibodies) ```
41
CD28
T cell surface molecule Interacts with B7.1 (CD80) and B7.2 (CD86) on APC Important in providing second signal to activate naiive T cells Lack of interaction can lead to anergy Counterpart to CTLA-4
42
CTLA-4
T cell surface molecule Constitutively expressed on TRegs and induced on activated T cells Also interacts with B7.1 and B7.2 Acts to switch OFF T cell function (downregulates)
43
TCR
Heterodimer consisting of a or B chain Both chains anchored in cell membrane Like Ig, T cell receptor consists of variable and constant region Constant: AA that are the same across lots of different receptor types Variable: variability that can interact with antigen TCR genes do not undergo somatic hypermuation T cell does not develop further after it leaves thymus TCR requires CD3 function to function
44
Somatic Hypermutation
In B cells Additional nucleotide substitutions take place during activation and division of the cells Some of these substitutions result in better binding between Ig and antigen These B cells are then clonally expanded (Further rearrangement after B cells leave the bone marrow to get extra variability) *T cells do NOT do this*
45
Cellular Interactions between B and T cells
Neither usually act in isolation B cells require T cells to function T cells require APC to present antigen to them
46
BCL-2
Gene that encodes for BCL-2 protein Expression of BCL-2 inhibits apoptosis and is found in certain lymphomas; overexpression could lead to malignancy Particularly B cell follicular lymphoma *Regulation of Hematopoiesis* Aka production of cells out of bone marrow
47
FAS
Encodes for FAS protein When Fas interacts with its ligand, FasL, apoptosis of the cell occurs *Regulation of Hematopoiesis* Aka production of cells out of bone marrow
48
Early development in Hematopoiesis (three precursors & life span)
Blood cells arise from a common pluripotent stem cell Three types of precursors 1. Erythroid progenitors (RBCs, platelets) [life span 120 days] 2. Myeloid committed precursor cells (neutrophils, eosinophils) [life span days or weeks] 3. Lymphoid committed precursor cells [can live for years]
49
Leukocytes
WBCs Adaptive and innate responses Originate in bone marrow Ability to recognize foreign invaders and destroy them
50
Three main groups of lymphocytes (and type of receptors)
B cells and T cells Both possess antigen receptors NK cells Don't have specific antigen receptors, making them a part of innate immune system. But they use ADCC (antibody-dependent cellular cytotoxicity aka utilizing antibodies to recognize specific antigens)
51
EBV
Affects B cells and causes them to divide Would grow exponentially unless they are regulated T cells normally regulate, can recognize that they're infected with a virus and kill them. When a T cell kills a B cell, you feel awful. AKA Mononucleosis Need this process thought because if the T cells didn't kill the B cells, you'd die
52
Co-dominant
MHC antigens are co-dominant | You express what you get from your mom and dad
53
Allelic exclusion
TCR and BCR Only get one T or B cell receptor expressed If one is expressed, the other stops working True allelic exclusion is relatively rare
54
Haplotype
Combination of alleles at linked loci found on one chromosome Often used with reference to MHC
55
Polymorphism (and of MHCI and MHCII, genetics)
Existence of multiple alleles at a particular gene locus MHCI: only have 6 MHCI molecules; only the a/heavy chain has polymorphism MHCII: a & B chains are polymorphic; and a & B chains can make different combos too; a lot greater diversity; for some people up to ~21 different MHCII molecules on a given APC Each individual inherits one allele from each parent BUT Not necessarily the same as your parents because you could have an a pair with different B that's different
56
Specificity of (broad and precise) Antigen with MHC and TCR / vaccines
Antigen binds to MHC with broad specificity Antigen binds to TCR with precise specificity Because we only have a limited number of MHC molecules, there could be an antigen that we can't present. As vaccines become more precise, we could possibly have someone that can't present antigen to T cells Ex. HepB vaccine can't be presented by certain individuals; it can't sit in the MHC cleft Even a good vaccine will only work on about 90% of population
57
CD34+
Stem cells in the bone marrow Precursors ot thymocytes Crucial because indicator of a stem cell The molecule they use to pull the stem cell out in transfusions
58
Positive Selection
Functioning T cells must be able to bind to MHC complex If DP cells bind to MHCI, they become CD8+ SP cells If DP cells bind to MHCII, they become CD4+ SP cells Cells that cannot bind undergo apoptosis
59
Negative Selection (and goldilocks idea)
For potential disease causing cells That could respond to self antigen presented by MHC Goldilocks idea: Thymocytes that do not bind to MHC do not survive Thymocytes that bind to self MHC and self antigen are also destroyed Those with intermediate affinity survive
60
Central Tolerance
Occurs in thymus | Cells that respond strongly to self MHC and self antigen are destroyed
61
Peripheral Tolerance
When self reacting T and B cells are in an unreactive state to self antigens When cells leave the Thymus, they need to learn not to respond to our own antigens (like food or microbial antigens)
62
Mechanisms of Peripheral Tolerance
1. Ignorance: Autoreactive T cells never encounter their cognate Ag except by accident Ex. Orchitis: Patient with mumps; inflammation of vesicles in testes which allows lymphocytes to go through there; they can become sterile because lymphocytes encounter sperm for the first time and mount an immune response to them 2. Deletion: Self-specific peripheral T cells are destroyed after TCR engagement; Negative selection is leaky though 3. Anergy: State of unresponsiveness induced upon self-Ag recognition 4. Foxp3+ Treg cell-mediated suppression of dangerous T cell responses against self-Ag Prevent autoimmune responses
63
Treg
Possess high levels of FoxP3 and CD25 (part of IL-2 receptor) Produced by stimulating CD4+ T cells with TGFB (transforming growth factor beta) Can inhibit T cells via cytokines >IL-10 and TGFB (can switch off other T cells)
64
Why might live viral vaccines have complications causing disease in patients with T cell defects?
There would be no immediate response to vaccination. Defects in antibody production from B cells may hinder long term protection from the vaccine but would not lead to acute infection from vaccination
65
Surface makers on NK cells
CD16/56

Immunity (3 decks)

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