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T cell, autoimmune, hypersensitivity Flashcards

1
Q

T cells

A

CD8 cytotoxic
class I

Cd4 T helper
class II

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2
Q

TCR

A

no somatic hypermutation as can lose ability to recognise MHC otherwise
monovalent
membrane bound
antigen recognition
more variable than BCR

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3
Q

TCR diversity

A

2 chains Beta and alpha
VDJ rearrangement
Beta chain first
Dj then VJ
CD4, CD8 double negative expressed

Then alpha chain rearranged
CD4, CD8 double positive expressed

RAG 1/2 P and N nucleotide addition

As no somatic hypermutation needs more diversity as fixed

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4
Q

T cell selection

A

successful TCRβ chain rearrangement

Positive selection
double positive TCR against self peptide/MHC on cortical epithelial cells
Only cells with no affinity die as no positive survival signals
Depending on the MHC T cell becomes single positive

NEgative selection
Remove T cells with high affinity for self peptide/MHC by apoptosis

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5
Q

Thymus

A

cortical epithelial cells for positive selection

(dendritic cells and macrophages to trigger negative selection

Macrophages are important for removing
thymocytes that fail to mature

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6
Q

TCR signalling

A

TCR can only be expressed with CD3
Once bound to MHC Lck binds CD8/4
CD3 phosphorylated by Lck
recruits ZAP-70
ZAP-70 phoshporylates LAT
LAT gets PLCgamma and GRB2
GRB2 gets SOS, activates RAS and MAPK pathways RAF,MEK,ERK
Activates transcription factors including IL-2

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7
Q

Cytotoxic T cell

A

CD8 T cell recognise MHC class I
Proliferate with IL-2 and also make perforin and granzyme

Release IFN gamma to increases expression of MHC

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8
Q

Il-2

A

Master T cell regulator
Cause T cell survival and proliferation

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9
Q

Co stimulation

A

T cells need 2 signals

signal 1
TCR and MHC
with CD4/8

signal 2
CD28 with B7 on APC for signal and
CD40L with CD40 on APC to activate APC

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10
Q

Thymus dependent antigens

A

APC, dendrite takes up antigen and presents on MHC
Presents to T cell
MHC class II-TCR and CD4
B7-CD28
CD40-CD40L

T cell activates B cell
CD40L-CD40
CD28-B7
TCR,CD4-MHC

B cell can take up antigen and present on MHC, when T cell binds it recognises to help activate

CD28-B7
CD40L-CD40
signals needed for survial and proliferation-CD40

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11
Q

Germinal centres

A

follicular
dendritic cells hold antigens for a long time on immune complexes

Somatic hypermutation occurs so only B cell with highest affinity after muations survive

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12
Q

Thymus independent antigens

A

TI antigens are microbial products
composed of repetitive elements (polysaccharides and lipopolysaccharides) which crosslink membrane Ig and induce B cell proliferation.

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13
Q

T helper 1

A

Made by IL-12 and IFN-γ
Make IFN-γ, inflammation
activate phagocytes

T-BET
ILC1

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14
Q

Th2 cells

A

Made by IL-14
Make IL-4, IL-5 and IL-13
Help against parasites

Parasite too big for phagocytosis, mostly antibodies made

GATA3
ILC2

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15
Q

Th17 cells

A

Made by IL-6 and TGF-β
Make IL-17 and IL-22
extracellular bacteria and fungi

RORγT
ILC3

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16
Q

Follicular helper T (Tfh) cells

A

MAde by IL-6
MAke IL-21
promtoe antibody response

small amount so B cells compete and only highest affinity survive

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17
Q

Treg

A

made by TGF-β
supress the activity of other T cells

FOXP3.

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18
Q

Innate lymphocytes

A

Similar to T helper cells
act before T helper cells

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19
Q

Memoery cells

A

Some T/B cells develop long lived cells that cause a secondary response that is faster and greater in magnitude than the first

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20
Q

Tolerance

A

aquired
recognise infectious non-self

need adjuvant, PAMPs and DAMPS as well as antigen

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21
Q

Central tolerance

A

First make T cell receptors
positively selecting those clones with some
affinity for self MHC and negatively selecting clones that bind too strongly to self MHC
plus peptide

timing, dose of antigen,
amount of costimulation and location are important

A mouse A with bone marrow from B at borth accept a skin graft from B but not from C

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22
Q

How can all relevant self antigens be expressed in the thymus?

A

transcription factor called AIRE
Turns on pheripheral genes in the thymus so T cell see all genes

Without AIRE
Autoimmune Polyglandular Syndrome Type
1 (APS-1)
or APECED

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23
Q

B cell tolerance

A

B cells that react to abundant antigens on self cells are
eliminated as they develop

Self-reactive cells have an opportunity to avoid apoptosis by
replacing the light chain in a process called receptor editing, recombination

HIgh doses of self antigen cause anergy induction in spleen
non resposnsive

24
Q

T cell tolerance
Ignorance

A

Ignorance
immunologically privileged sites include the brain,
eye, placenta and testis cant be reaced by cells, can be damaged

blood brain barrier

Testes sperm are halpoid so T cells have never seen them before so need to be protected

25
T cell tolerance Pregnancy
foetus and placenta share the child’s genotype Physical barrier to the mother’s T cells Lack of MHC class I expression on outer placenta Production of immunosuppressive factors such as α-fetoprotein and IDO (indoleamine 2,3-dioxygenase, a tryptophan catabolising enzyme
26
T cell tolerance Split tolerance
T cell tolerance has been established but autoreactive B cells are still present. Without T cell help the B cells are 'helpless.
27
T cell tolerance Anergy
If T cell only binds MHC and no costimulatory B7 and CD40 No longer responds to anything PAMPs cause dendritic cells to express B7 and go to the lymph node dendritic cells not activated anergise T cells
28
T cell tolerance Treg supression
On contacting self antigen presented by MHC class II molecules Tregs suppress the proliferation of naive T cells responding to autoantigens Use IL-10 and TGF-β Produce IDO decrease B7 expression on APCs using CTLA4 which has higher affinity than CD28 Kill T cells by perforin and granzymes Take up all availabe IL-2
29
T cell tolerance T cell exhaustion
Exhausted T cells express the co-receptor PD1 and CTLA4 PD! binds PD-L1 and PD-L2 which causes suppression of T cell signalling Anti PD1 and CTLA4 are cancer treatment
30
Experimental tolerance
Abetacept is an engineered soluble form of CTLA4 removes CD28, T cell cant get costim so dont function
31
Cancer decreasing toleracnce
Tumours have lost MHC Ipilimumab is an antibody against CTLA4, block CTLA4 and so allows more T cells to be activated CAncer can make PD-L1 which deactivated T cells so anti PD1 or PD-L1 can be used
32
Autoimmunity
Autoimmunity is an excessive adverse immune response against self-antigens
33
Autoimmunity disease
Organ specific- Graves diseas Systemic- Systemic Lupus erythematosis affects every organ
34
Hypersensitivity
Hypersensitivity types II (antibody) Type III (immune complex) IV (cell-mediated)
35
Graves disease Antiobody
TSH binds TSH receptors stops thyroxine production Antobody binds TSH, overproduction of thyroxine hyperthyroidism Hashimoto thyroditis- antibody binds thyroid peroxidases, TSH receptor, decreased production of thyroxine
36
Myasthenia Gravis Antiobody
Antibodies block acetylcholine receptor Receptor internalise and degraded and less responsive Can't perform long muscle contraction
37
Immune complex mediated effects.
Complement binds immune complex Then binds to complement receptor 1 on erythrocytes Taken to liver and spleen, phagocytosed If not removed deposition occurs, can damage
38
SLE (systemic lupus erythematosus), Immune complex
wolf rash on face Have a wide variety of anticytoplasmic and anti-nuclear auto-antibodies Lots of immune complexes made and deposited everywhere, recruits lots of complement In kidney complexes get stuck in glomerulus, damage complement deficiencies that impair immune clearance, such as C1, C2, C4 are predisposing factors
39
T cell-mediated (cellular autoimmune) diseases
Multiple Sclerosis (MS) T cells cross the blood-brain barrier damage myelin sheath Central nervous system demyelinated Impaired nerve transduction and hence impaired mobility In mice transmitted by transferring T cells Type 1 Diabetes (T1D) insulin-producing β cells destroyed by T cells blood glucose levels can become dangerously high, causing neurological and vascular damage. Rheumatoid arthritis (RA) CD4 T cells destroy joints
40
GEnetic factors causing autoimmune disease
HLA allotype can predispose HLA B27 causes 9/10 people to have ankylosing spondylitis, 150x risk Due to binding different peptide in MHC
41
Endocrine factors (sex differences) causing autoimmune disease
Females more susceptible due to hormone pregnancy can make it better or worse
42
Environment and microbes causing autoimmune disease
Streptococcal infection can cause rheumatic fever as cell wall similar to heart valve protein so attacked Molecular mimicry Epstein Barr virus causes multiple sclerosis Ethnicity also a factor
43
Potential triggers and causes of autoimmunity
Proteins like gluten modified by enzyme so MHCII picks it up in Coeliac disease protein citrullination by peptidylarginine deiminase causes Rheumatoid arthritis (RA) starts in lung due to smoking ACPA (anti-citrullinated protein antibodies) are present in patients
44
Treatments
thyroxine for hypothyroidism and insulin for type-1 diabetes. Immunosuppressive drugs like steroids immunosuppressive agents include cyclosporin and rapamycin. These are potent inhibitors of T cell activation. Antibodies for TNF-α or its receptor have proved to be effective in RA as TNF-alpha inflammatory CTLA4 to treat RA by removing B7 so no costim for T cells
45
Type I hypersensitivity IgE mediated
Hypersensitivity is extreme response to foreign agent autoimmune to self IgE mediated Sensitivity when dendritic cell presents antigen to T cell, becomes TH2, activates B cell and makes antibodies asthma pollen anaphylaxis-peanuts IgE binds antigen binds to Fc receptor on mast cell Cross links 2 receptos degranulation histamine release-inflammation Test by skin prick, causes wheal (swelling), flare(redness) due to increased blood flow Genetic inheritance, susceptible parents doubles risk for child
46
Asthma
Increased TH2 lymphocytes amplify inflammation and airway remodeling constrict the bronchial smooth muscle to attempt expulsion of the offending material by coughing a late response follows after about 6 hours, due to leukotrienes, most damaging Breathing test after exposure Desensitization therapy by giving small amounts of antigen
47
Type II hypersensitivity Antibody mediated
IgM or IgG antibody binding destroying rbc or platelets Blood transfusion ABO O-umnodified H antigen A-adds a terminal N-acetylgalactosamine B-adds a terminal galactose AB both You pre existing antibodies to the sugars you dont have O can donate to all as no antigen on blood A only to A or AB as O and B have anti B Same for B
48
Type II Rhesus reaction Rhesus antigen on RBC
RhD- mother makes anitbodies for Rhesus antigen DUe to RhD+ cells from child leaking into mother, only happens during birth so problem for second child IgG can cross placenta and harm child anti-Rh antibody (RhoGam) usedto eliminate Rh anitgen in leaked child cells before mother responds Mother B cell Fc receptors may be cross linked and tolerised
49
Type III Hypersensitivity Immune-complex mediated
IgG hypersensitivity when antigen is soluble and in high quantities so foms complex trigger mast cells visa FcgammaRIII receptor Complement C5a prime mast cells to respond to immune complexes of anitgen MAst cells degranulate, histamine release, inflammation Serum sickness when horse serum was used to treat pneumonia
50
Type IV hypersensitivity T cell mediated
Delayed type hypersensitivity Needs high dose of antigen,10-100 times more TH1 cells release cytokines, after 48-72hours and recruit macrophages causing damage Due to haptens-antigens which forms complexes with host proteins Activate TH1 metal, poison ivy
51
The Mantoux test for Mycobacterium tuberculosis exposure
inject a small amount of tuberculin under the skin T cells will recognise the inoculum and mediate a type-I immune response leading to oedema(visible lesion) Vaccinated people also respond
52
Transplants
Mostly allogenic, from same species, second graft rejected faster due to memory T cells
53
HYperacute rejection
results from pre-existing antibody due to previous transplant pregnancy blood transfusion Complement and immune complexes form and clog blood vessels, Fast
54
Acute graft rejection
barrier to allotransplantation. Direct recognition T cells recognise allogenic MHC and respond Cytotoxic T cell killing Not an issue in blood transfer as rbc no MHC Indirect recognition APC take up allogenic protein, present to T cells which react
55
Chronic Rejection
IgG antibodies against allogeneic HLA class form immune complexes that block blood vessels
56
Other transplants
In immuno privleged sites work well Haemopoietic stem cell transplants Host immune system destoryed by chemo, donor stem cells added graft versus host (GvH) as donor T cells react with host HLA Autologous transplant, own cacnerous stem cells removed, tumour removed and put back in Relapse

BOD (5 decks)

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