Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immunity > T-Cells: Development and Activation > Flashcards

T-Cells: Development and Activation Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Three functions of T lymphocytes

A
  1. Production of cytokines
  2. Cytotoxicity (kill other cells)
  3. Control of other immune cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MHC I

A

Found on all nucleated cells

Present antigen to CD8+ (Tc)

Saying “kill me”

HLA-A, HLA-B, HLA-C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which MHC molecules are found on macrophages?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Chronic Wuchereria Bancrofti Infection

A

After many years of infection

Microfilaria block lymphatic vessels, resulting in edema in legs, scrotum, and breasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Lymph Node (APCs, 3 parts, blood supply)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

B cells > Plasma cells

A

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
Q

Spleen

A

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
Q

Other lymphoid tissues

A

(Spleen, Thymus)

Appendix
Tonsils
Adenoids
Peyer’s patches

30
Q

GALT

A

Gut associated lymphoid tissue

Peyer’s patches
Appendix

GALT+BALT = MALT
Mucosal-associated lymphoid tissue

31
Q

BALT

A

Bronchial associated lymphoid tissue

Respiratory tract lymphoid tissue

GALT+BALT = MALT
Mucosal-associated lymphoid tissue

32
Q

How are antigens transported from mucosal surfaces to the lymphoid system?

A

M cells:

Microfold
Membranous cells

33
Q

Lymphocyte Recirculation

A
  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
Q

Langerhans cells

A

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
Q

TCRgd cells

A

Intraepidermal lymphocytes that are thought to be a first response to infection

36
Q

Definition of Antigen

A

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
Q

Haptens

A

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
Q

Adjuvant

A

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
Q

T Cell Epitopes

A
  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
Q

CD40L (ligand)

A

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
Q

CD28

A

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
Q

CTLA-4

A

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
Q

TCR

A

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
Q

Somatic Hypermutation

A

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
Q

Cellular Interactions between B and T cells

A

Neither usually act in isolation

B cells require T cells to function

T cells require APC to present antigen to them

46
Q

BCL-2

A

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
Q

FAS

A

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
Q

Early development in Hematopoiesis (three precursors & life span)

A

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
Q

Leukocytes

A

WBCs

Adaptive and innate responses

Originate in bone marrow

Ability to recognize foreign invaders and destroy them

50
Q

Three main groups of lymphocytes (and type of receptors)

A

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
Q

EBV

A

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
Q

Co-dominant

A

MHC antigens are co-dominant

You express what you get from your mom and dad

53
Q

Allelic exclusion

A

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
Q

Haplotype

A

Combination of alleles at linked loci found on one chromosome

Often used with reference to MHC

55
Q

Polymorphism (and of MHCI and MHCII, genetics)

A

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
Q

Specificity of (broad and precise) Antigen with MHC and TCR / vaccines

A

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
Q

CD34+

A

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
Q

Positive Selection

A

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
Q

Negative Selection (and goldilocks idea)

A

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
Q

Central Tolerance

A

Occurs in thymus

Cells that respond strongly to self MHC and self antigen are destroyed

61
Q

Peripheral Tolerance

A

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
Q

Mechanisms of Peripheral Tolerance

A
  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
Q

Treg

A

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
Q

Why might live viral vaccines have complications causing disease in patients with T cell defects?

A

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
Q

Surface makers on NK cells

A

CD16/56

Immunity (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions