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Host Defense Exam 1 > T Cell Maturation > Flashcards

T Cell Maturation Flashcards

1
Q

What kind of T cells can HSCs develop into?

A
  • NK T cells
  • T Regulatory cells
  • Cytotoxic T cells (CD8+)
  • Helper T cells (CD4+)
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2
Q

Describe the development of the thymus in utero.

A

Week 4-7: Derived from the pharyngeal pouch, the thymic gland breaks off bilaterally and travels to the mediastinum. Forms a single bilobule pouch

Week 7: colonization by HSCs
Week 12: production of T cells
Week 13: mature T cells egress
birth: large repertoire of peripheral T cells

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3
Q

Describe DiGeorge Syndrome (AKA?)

A

AKA velo-cardio-facial syndrome (VCFS)

  • due to deletion of chromosome 22
  • symptoms = no hair, characteristic facial features, heart defects, recurrent infection
  • manifestation = no thymus, no T cells
  • severe immunodeficiency
  • tx = thymus graft transplant
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4
Q

Describe FOXN1 mutation.

A
  • FOXN1 gene on chromosome 17
  • normal function = encodes a transcription factor essential for TEC development
  • mutation = CGA => TGA (stop codon)
  • in utero, immature epithelial progenitors form cyst-like thymus, cannot recruit HSCs
  • symptoms - immunodeficiency
  • tx - thymus transplant
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5
Q

What kind of cells make up the thymic capsule?

A

fibroblasts

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6
Q

What kind of cells make up the thymic cortex?

A

developing T cells, some macrophages, cortical TEC

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7
Q

What kind of cells make up the thymic medulla?

A

mature T cells, macrophages/DCs, medullary TEC

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8
Q

What kind of cells make up the CMJ?

A
  • macrophages and DCs

- entrance of thymocyte progenitors

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9
Q

What is the purpose of the cells in the CMJ?

A
  • macrophages and DCs
  • APC
  • negative selection
  • phagocytosis of apoptotic thymocytes
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10
Q

Which cells make up the thymic stroma?

A
  • fibroblasts

- TEC

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11
Q

What are the kinds of TEC?

A
  • cortical
  • medullary
  • Hassal’s
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12
Q

What are TEC derived from?

A

endoderm

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13
Q

What cytokines do TEC produce?

A
  • IL-1, IL-6, IL-7
  • stem cell factor (SCF)
  • thymic stroma lymphopoietin (TSLP - used for Treg differentiation)
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14
Q

What surface markers do TECs have?

A
  • Delta-like-1, Delta-like-4
    (required for notch signaling and T lineage commitment)
  • MHC I and II (positive selection)
  • peripheral tissue antigens (negative selection)
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15
Q

In what form do HSCs enter the thymus?

A

CD34+

via blood

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16
Q

What cell is the umbilical cord rich in?

A

CD34+

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17
Q

What happens to T cell proliferation after puberty?

A
  • declines, but peripheral pool is maintained
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18
Q

What are the stages of T cell development?

A
  1. T lineage commitment
  2. Proliferation
  3. Differentiation
  4. Positive Selection
  5. Negative Selection
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19
Q

What are the cell stages of T cell development?

A
  • progenitors
  • pre-T
  • ISP
  • DP
  • mature SP
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20
Q

Describe the mechanism of T cell lineage commitment.

A
  1. thymocyte progenitors from the bone marrow enter the thymus via blood
  2. Notch ligand on the progenitor interacts with DL1 or Dl4 on cortical TECs
  3. notch-delta signaling terminates possibility of other lymphoid lineages and commits cell to T lineage
21
Q

Describe how a progenitor becomes a pre-T cell.

A
  1. after notch-delta signaling, committed progenitors express CD1A
  2. Through CD1A and IL-7, cell begins expressing RAG 1 and RAG2 and undergoes TCR-gamma, delta, and beta rearrangements
  3. expression of the pre-TCR complex (pTa, rearranged B chain, CD3)
22
Q

Describe how a pre-T cell becomes an ISP.

A
  1. After pre-TCR complex is expressed, CD4 is expressed

Now it is an immature single positive cell

23
Q

Describe ISP Beta selection stage.

A
  1. At this stage, the ISPs express CD3, CD4, and a pre-TCR complex
  2. Once a functional cell is selected => degradation of RAG to stop further beta chain rearrangement
  3. vigorous proliferation of the ISPs (huge increase in thymocyte numbers)
  4. increase expression of CD3
24
Q

What is the purpose of ISP Beta selection?

A

The purpose of this stage is to positively select for functional B chains

25
Q

How does an ISP become a DP?

A
  1. beta selected cells now express both CD4 and CD8
  2. re-expression of RAG induces alpha chain rearrangement (deletion of delta genes)
  3. mature alpha and beta TCR
26
Q

What is unique about alpha chains in TCR?

A

no allelic exclusion
more than one alpha chain can bind to the same beta chain
thus, one DP might express multiple alpha chains

27
Q

Describe the process of positive selection.

A
  1. cTECs express both self-MHC and self-peptide (peptide:MHC complex)
  2. If a DP binds to MHC Class I => downregulation of CD4+ => becomes a CD8+ T cell
  3. If a DP binds to MHC Class II => downregulation of CD8+ => becomes a CD4+ T cell
  4. If a DP does not bind OR binds too strongly => apoptosis (induced by CMJ cells and phagocytosed by those as well)
28
Q

What is BLS?

A

Bare Lymphocyte Syndrome

  • defect in MHC Class II expression
  • cannot produce CD4+ cells
29
Q

Why is positive selection important for bone marrow transplant recipients?

A
  • the patient did NOT receive a thymic transplant.
  • Therefore, the cTECs still express SELF-MHC
  • donor bone marrow progenitors will be selected for based on affinity to self-MHC instead of donor-MHC
30
Q

Describe the process of negative selection.

A
  1. mTECs encode AIRE, a transcription factor that induces expression of various organ-specific antigens
  2. T cells that bind with high affinity to the mTECs undergo apoptosis via CMJ or medullary macrophages/DCs
31
Q

Define AIRE.

A

autoimmune regulatory element

TF that encodes a battery of organ-specific self antigens

32
Q

Describe APECED.

A

autoimmune polyendocrinopathy candidiasis ectodermal dystrophy

  • mutation in AIRE
  • generation of several autoreactive T cells
  • symptoms = candidiasis, candidal onychomycosis, vitiligo, halo neevi
  • affected organs = adrenal, thyroid, parathyroid, pancreas
33
Q

What are some AIRE mutations?

A

APECED

APS1

34
Q

What do T-gd cells derive from?

A

ISP

35
Q

What is unique about T-gd cells?

A
  • double negative for CD4/CD8
  • can bind antigens directly
  • do not need MHC presentation
36
Q

Describe T-gd1 cells.

A
  • reside in epithelial tissue

- recognizes stressed tissues and lipid antigens present on CD1B or C

37
Q

Describe T-g9-d2 cells

A
  • circulating T-gd cells
  • recognizes phosphor antigens found on mycobacterium and malaria
  • immunoregulation
38
Q

Define CD1

A
  • related to MHC
  • ABCD
  • BC mostly bind to glycolipid antigens
39
Q

Describe development of NKT cells.

A
  • derived from DP thymocytes that recognize glycolipids:CD1D on cTECs
40
Q

Describe surface markers of NKT cells.

A
  • express both TCRab (T cell) and CD25+ (NK)

- can be CD4+ or double negative

41
Q

Where do NKT cells reside?

A
  • reside in spleen, lymph nodes, bone marrow
42
Q

List NKT functions.

A 
- immunoregulation
Th1 cytokines (IFN-g, IL-2) => increases cytotoxicity of NK and killer T cells, increases macrophage phagocytosis, increases Th1 response

Th2 cytokines (IL-4, IL-10, IL-13) => increase Th2 response

43
Q

Define dominant tolerance.

A

suppression of autoreactive T cells by Tregs instead of apoptosis (like by central tolerance)

44
Q

What is the function of Tregs?

A

suppress autoreactive T cells that escaped from central tolerance

45
Q

What do Tregs express?

A

CD4+CD25+

46
Q

What cytokines are required for Treg development?

A
  • derived from peripheral mature CD4+ T cells
  • TGF-b
  • TSLP (thymic stroma lymphopoietin)
  • creates Tr1 and Th3
  • FOXP3
47
Q

Describe IPEX.

A

immune dsyregulation, polyendocrinopathy, enteropathy, x-linked

  • multisystem autoimmune disease
  • symptoms - diarrhea, insulin-dependent DM, thyroid, eczema
  • due to FOXP3 defect
  • lacks Tregs
48
Q

What can abnormal Treg levels lead to?

A

too little = IPEX

too much = cancer

Host Defense Exam 1 (12 decks)

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