T Cells

T cells, also called T lymphocytes, are important components of the adaptive immune system. Production starts from the hematopoietic stem cells in the bone marrow, from which T-cell progenitor cells arise. These cells migrate to the thymus for further maturation. A functional mature T cell develops from a step-by-step process creating a T-cell receptor (TCR) complex, selecting T cells with appropriate affinity to self-antigens associated with major histocompatibility molecules (positive selection), and expressing either CD4 or CD8. In this series, cells predisposed to autoimmunity undergo apoptosis (negative selection). When released from the thymus, the naive mature T cells travel to the secondary lymphoid organs for activation. Two signals, an antigen-specific binding of TCR and costimulation, are required to be activated (ready to mount an immune response). In the case of CD8+ T cells, additional cytokine stimulation is necessary. Depending on the cytokines they are exposed to during antigen stimulation, the undifferentiated mature T cell (Th0) develops into cells with different functions: CD4+ become T helper (Th) cells and CD8+ become cytotoxic, or cytolytic, cells. Th cells have other subtypes; the most characterized are Th1, Th2, Th17, follicular Th cells, and regulatory T cells. Other types include natural killer T cells and memory T cells. These mature differentiated T cells ensure effective surveillance and immediate response to pathogens, tumor cells, and foreign tissues and provide immunologic memory.

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T-Cell Development

Introduction

  • T (thymus-derived) cells: responsible for cell-mediated immunity
  • Production: hematopoietic stem cells (in the bone marrow) → common lymphoid progenitor → early thymic progenitor cells → thymus
  • In the thymus:
    • T cell progenitors are seen by 9 weeks of gestation.
    • The developing T cells in the thymus are also called thymocytes.
    • Gene rearrangements take place to form the T-cell receptor (TCR):
      • The majority (> 85%) of T cells contain chains ɑ and β, as well as 1 of the co-receptors CD4 or CD8.
      • The remaining T cells contain chains ɣ and δ.
      • TCR + CD3 form the TCR complex.
      • CD3: marker most commonly used to identify T cells 

Development

The initial process takes place in the outer cortex of the thymus, and the cells move into the deeper cortex as they mature. 

  • In the thymus, progenitor cells express CD3 but lack cell-surface expression of CD4 and CD8 molecules, thus are double-negative (DN) cells/thymocytes. 
  • The TCR genes of these DN cells are rearranged.
    • Like immunoglobulins, TCR proteins are encoded in following gene regions:
      • Variable (V)
      • Diversity (D)
      • Joining (J)
      • Constant (C)
    • The β chain has VDJ rearrangements, which involve the antigen-binding site.
    • The ɑ chain involves VJ rearrangements in the antigen-binding site.
    • Rearrangements also occur in a minority of T cells with δ and ɣ chains.
    • This process gives rise to TCR diversity.
  • There are 4 DN stages, and these can be distinguished by the expression of CD44 and CD25:
    • DN1: CD44+,CD25–
    • DN2: CD44+,CD25+
    • DN3: CD44–,CD25+
    • DN4: CD44–,CD25–
  • By stage DN3, rearrangements of the β chain occur (pre-TCR); failure to do so results in apoptosis.
  • By DN4, ɑ-chain gene rearrangements is completed:
    • With this, signals are produced to move forward with maturation. 
    • Rearrangement of the TCR α-chain genes corresponds to the up-regulation of both CD4 and CD8 expression (becoming double-positive (DP) cells).
    • If ɑ-chain gene rearrangements do not occur, the cell dies.
  • The α–β TCR–CD3 receptor complex is completed when ɑ chains assemble with β chains.
  • Subsequent maturation stages:
    • Positive selection:
      • In the thymic cortex
      • T cells with TCR having moderate interaction (just enough affinity) with self-antigens (in the context of MHC molecules) are selected.
    • Negative selection:
      • In the medulla
      • T cells with TCR with high affinity or strong interaction with self-antigens → apoptosis
      • This central tolerance mechanism (in the thymus) is where T cells that react strongly to identified self-antigens are removed.
      • Prevents release of dysfunctional T cells (that recognize self-antigens and can activate autoimmunity)
      • Facilitated by autoimmune regulator (AIRE) protein

Stages

To reach functionality, the T cell goes through stages, released from the bone marrow as progenitor cells to continue development in the thymus. The table summarizes the general steps taken. 

  • In the initial stages, the aim is to build the receptor (requiring no antigen). 
  • Further steps involve the interaction of the T cell with self-antigens, and differentiation into either T helper cells or cytotoxic T cells.
Table: T-cell maturation stage
Maturation stageT-cell receptorAssociated events
Progenitor cellNone
  • From bone marrow → to the thymus for further maturation
  • Become DN cells (still lacking CD4 and CD8)
DN cellsRearrangement of β chain (pre-TCR): failure to rearrange leads to apoptosis
  • Express CD3
  • CD4–, CD8– (no CD4 and CD8)
DP cellsRearrangement of ɑ chain → ɑ chains assemble with β chains → complete ɑ–β TCR–CD3 receptor complex (expressed on the surface)
  • CD4+, CD8+
  • DP cells then interact with self-antigens (in the context of MHC molecules).
  • With MHC presentation, some cells undergo positive selection in the thymic cortex:
    • Intermediate or moderate interaction between MHC and TCR occurs.
    • Produces the functional cells
  • Some cells undergo negative selection in the thymic medulla:
    • High affinity or strong interaction between MHC and TCR occurs.
    • Cells die (apoptosis).
    • Prevents release of dysfunctional T cells (can activate autoimmunity)
  • Some fail to interact → apoptosis
Single positive T cells
  • Cell signals trigger cells to express either CD4 or CD8, not both:
    • Th: with CD4 and interact with cells expressing MHC class II
    • Tc: with CD8 and interact with cells expressing MHC class I
  • Naive Th and Tc circulate (blood to lymphoid tissues to lymph), and await activation by antigen-presenting cells carrying a complementary peptide–MHC complex.
Tc: cytotoxic T cells
Th: T helper cells
T-cell differentiation stages

Differentiation stages of T cell:
From the bone marrow, progenitor cells go to the thymus for further maturation. The DN cells (no expression of CD4/CD8 or CD4–/CD8–) have not developed the TCR. The DN cells undergo rearrangement of the TCR gene and become pro-T cells, then pre-T cells. Through the series, CD4 and CD8 are expressed, and the TCR becomes assembled through gene rearrangements (DP cells). The thymus then presents MHC molecules to the developing T cells. Some cells undergo positive selection (intermediate interaction between MHC and TCR takes place) and produce functional cells. Some cells undergo negative selection (strong interaction between MHC and TCR), which results in cell death. The release of dysfunctional T cells, which can activate autoimmunity, is prevented. Some T cells fail to interact, leading to apoptosis. Mature T cells express either CD4 (T helper cells) or CD8 (cytotoxic T cells), not both.

Image by Lecturio. License: CC BY-NC-SA 4.0

Mnemonic

Remember the “rule of 8”

  • MHC restriction: The T cell is “restricted” to bind an antigen only when it is presented by the appropriate class of MHC protein.
  • CD4-positive T cells recognize antigen associated with class II MHC proteins (4 × 2 = 8).
  • CD8-positive T cells recognize antigen associated with class I MHC proteins (8 × 1 = 8).

T-Cell Activation and Differentiation

Release from the thymus

  • Before T cells emerge from the thymus, they have interacted with self-antigens, undergone MHC restriction, and either have CD4 or CD8 expression.
  • The released T cells expressing surface α–β TCR–CD3 complex with co-receptors CD4 or CD8 are considered naive mature T cells: 
    • Not enough for proliferation and activation, as the released T cells have not interacted with a foreign antigen
    • These T cells circulate in the blood and go to the secondary lymphoid tissues.
    • These secondary lymphoid organs (e.g., lymph nodes) filter antigenic material, allowing the naive mature T cells to:
      • Interact with antigen-presenting cells, such as macrophages or dendritic cells
      • Sample the antigens to become activated
    • If no activation takes place, the T cells recirculate.
Structure and functional regions of a lymph node

Structure and functional regions of a lymph node comprising a collagen-rich fibrous capsule and an underlying subcapsular sinus.
Cells are segregated into (1) the cortex (consisting of B cells, T follicular helper cells, and follicular dendritic cells arranged in primary follicles, in which B cells survey antigens presented on the follicular dendritic cell stromal network); and (2) the paracortex (accommodates T cells, dendritic cells, and fibroblastic reticular cells, which form stromal cell networks and reticular fibers).
The inner medulla is composed of lymphatic tissues (medullary cords) separated by medullary sinuses consisting of lymph.

Image: “The structure of the lymph node” by Colbeck, Ager, Gallimore and Jones. License: CC BY 4.0

Activation

  • Full activation of T cells ready to mount an immune response requires 2 signals:
    1. TCR recognizes its cognate antigen, as presented by the antigen-presenting cell (e.g., dendritic cell).
    2. Costimulation:
      • Provided by a costimulatory molecule (e.g., CD28) 
      • Best characterized by B7 protein in the antigen-presenting cell interacting with CD28 of the T cell
      • Needed for survival and proliferation
      • Required to induce differentiation (effector or memory status)
      • Allows cell-to-cell cooperation
  • Without the costimulatory signal, the T cell can adopt a state of anergy (cell is alive but with partial or total unresponsiveness due to partial activation).
  • Effects:
    • Costimulation helps avoid activation of T cells by benign antigens.
    • In addition, CD8+ T cells, which are cytotoxic, require an additional “signal” given by cytokines from CD4+ T cells (preventing inadvertent activation).
  • Inhibitory mechanisms or “checkpoints” in T cells prevent uncontrolled T-cell activation:
    • Cytotoxic T-lymphocyte antigen-4 (CTLA-4)
    • PD-1 (programmed cell death-1)
2-signal model - T-cell dependence on costimulation

2-signal model of T-cell dependence on costimulation:
When both signal 1 (TCR binding the cognate antigen presented by the MHC molecule in the antigen-presenting cell) and signal 2 (costimulatory molecule interaction between the antigen-presenting cell and the T cell) are present, the mature T cell is fully activated.
The orange spot in the left panel indicates proper binding between antigen and TCR. However, when either signal 1 (middle image shows no antigen and TCR binding) or signal 2 (right image shows no costimulation) is missing, the T cell will not be fully activated.
Outcomes would be anergy (state of unresponsiveness), apoptosis (cell death), or ignorance (T cell does not notice or does not get affected by the antigen).
TCR: T-cell receptor

Image by Lecturio. License: CC BY-NC-SA 4.0

Proliferation and differentiation

  • Clonal proliferation: 
    • End of activation
    • Release of IL-2 (the T-cell growth factor) from the T cells leads to T-cell multiplication.
  • Depending on the cytokines that they are exposed to during antigen stimulation, the undifferentiated mature T cell (Th0) develops into cells with different functions:
    • CD4+ T cells become:
      • Follicular helper (Tfh) cells
      • Effector/helper T (Th) cells
      • Regulatory (Treg) or suppressor T cells
    • CD8+ T cells become cytotoxic T cells.
  • A number of activated T cells stay in the secondary lymphoid organ, and some proceed to areas of tissue inflammation to perform effector functions.

CD4+ T Cells

General overview of T helper cell differentiation

T helper cells have different cytokine profiles and roles in the immune response.

Table: General overview of Th cell differentiation
CD4+ T cellsDifferentiation stimulated byFunctionsCytokines produced
Th1
  • IL-12
  • IFN-γ
  • Activate macrophages
  • Activate cytotoxic T cells
  • IFN-γ
  • TNF
  • IL-2
Th2
  • IL-2
  • IL-4
  • Activate eosinophils, ↑ IgE
  • Activate mast cells
  • IL-4
  • IL-5
  • IL-6
  • IL-9
  • IL-10
  • IL-13
Th17
  • IL-1
  • IL-6
  • IL-23
  • TGF-β
Promote neutrophilic inflammation
  • IL-17
  • IL-21
  • IL-22
TfhIL-6Facilitate B-cell activation and maturation
  • IL-4
  • IL-21
Treg
  • TGF-β
  • IL-2
  • Suppress immune response
  • Promote self-tolerance
  • TGF-β
  • IL-10
  • IL-35
IFN: interferon
TGF: transforming growth factor
TNF:tumor necrosis factor
Subsets of CD4-+ helper T cells

Subsets of CD4-positive helper T cells:
After activation by a dendritic cell, in the presence of particular cytokines, a naive CD4-positive T cell divides and differentiates into effector/helper (Th1, Th2 or Th17) or follicular helper (Tfh) subsets. Each type of cell produces cytokines that facilitate activation of other immune-cell partners.
IFN: interferon
TNF: tumor necrosis factor

Image by Lecturio. License: CC BY-NC-SA 4.0

Th1

  • Differentiation stimulated by: IL-12 and IFN-γ
  • Inhibited by: IL-4 and IL-10 (from Th2)
  • Produce cytokines IFN-γ, IL-2, and tumor necrosis factor (TNF)
  • Express transcription factors T-BET and signal transducer and activator of transcription 4 (STAT4)
  • Functions:
    • Activates macrophages → enhanced phagocytosis, granuloma formation
    • Activates cytotoxic lymphocytes
    • Helps B cells produce antibodies
    • Inhibits Th2 cells
    • Defense against bacteria, fungi, and viruses
  • Clinical relevance:
    • Involved in delayed hypersensitivity reactions
    • Deficiencies in IL-12 or IFN-γ predisposes to mycobacterial infections, particularly tuberculosis.
    • Overactivity of Th1 cells: linked autoimmune and inflammatory diseases (e.g., Crohn’s disease, rheumatoid arthritis)

Th2

  • Differentiation stimulated by: IL-2 and IL-4
  • Inhibited by: IFN-γ (from Th1)
  • Produce cytokines IL-4, IL-5, IL-6, IL-9, IL-10, and IL-13
  • Express transcription factors GATA3 and STAT6.
  • Functions:
    • Activate eosinophils and mast cells
    • Inhibit Th1 cells
    • Help B cells
  • Clinical relevance: 
    • Dysregulation of Th2 cells leads to allergic disease (e.g., allergic asthma, atopic dermatitis).
    • Responds to infection by certain helminth worms, such as Schistosoma and Strongyloides

Th17

  • Differentiation stimulated by: IL-1, IL-6, IL-23, and TGF-β
  • Inhibited by: IL-4 and IFN-γ 
  • Produce cytokines IL-17, IL-21, and IL-22
  • Express transcription factors RORC and STAT3.
  • Functions:
    • Activate neutrophilic response
    • Barrier tissue defense
  • Clinical relevance:
    •  Increased susceptibility to mucocutaneous infections from the yeast Candida albicans in IL-17 deficiency 
    • Overactivity is associated with autoimmune disease.

Tfh

  • Differentiation stimulated by: IL-6
  • Inhibited by: IL-2
  • Produce cytokines IL-4 and IL-21
  • Express transcription factor Bcl-6.
  • Other markers: CXCR5, CXCL13, PD-1, and ICOS
  • Functions: 
    • Found in germinal centers of secondary lymphoid tissues and assist in the activation of B cells.
    • Expression of CD40 ligand (CD40L) interacts with CD40 of the B cell.
  • Clinical relevance: 
    • Mutation of the gene encoding CD40L leads to hyper-IgM syndrome.
    • Overactivity leads to autoimmune disease.

Tregs

  • Differentiation stimulated by: TGF-β and IL-2
  • Inhibited by: IL-6
  • Produce cytokines TGF-β, IL-10, and IL-35
  • Express transcription factor FOXP3.
  • Functions: 
    • Unrestrained T-cell response can become pathologic, so Tregs are present to prevent excessive inflammation and tissue damage.
    • Part of the peripheral tolerance mechanism
    • Can down-regulate the activity of many immune cells, including:
      • CD4+ cells
      • CD8+ T cells
      • Dendritic cells (via cell-surface CTLA-4 and lymphocyte-activation gene (LAG-3))
      • B cells
      • Natural killer cells
      • Eosinophils, basophils, mast cells
  • Clinical relevance:
    • Boosting Treg activity (or ↓ immune response) can help with transplant rejection and autoimmune disease.
    • Reducing Treg activity (or ↑ immune response) is helpful in cancer immunotherapy and chronic infections.
    • Significant role in preventing graft rejection and graft-versus-host disease (GVHD) 
    • Mutation of the gene encoding FOXP3 leads to IPEX (Immunodysregulation Polyendocrinopathy Enteropathy X-linked) syndrome.

CD8+ T Cells

  • Cytotoxic or cytolytic T cells
  • Requires cytokine (IL-2) stimulation (from Th1 cells) to be activated, then leaves the secondary lymphoid organ, circulating in search of targets
  • Produce cytokines IFNγ, TNF-α, and TNF-β
  • Express transcription factor RUNX3
  • Functions include killing of:
    • Pathogens
    • Infected cells
    • Tumor cells
    • Allografts
  • Cytotoxicity occurs via:
    • Granule exocytosis: 
      • Following contact with the target cell, lytic granules gather near the immunologic synapse. 
      • The membranes of the granules fuse with the cell membrane.
      • Granule contents, including granzymes and perforins, enter the target cell. 
      • Caspase pathway is activated, leading to apoptosis.
    • Expression of Fas ligand (FasL):
      • Fas is expressed on the surface of many cells.
      • FasL, expressed on the surface of CD8+ T cell, is induced when a cognate antigen is recognized.
      • Fas–FasL interaction ensues, caspase pathway is activated, leading to cell death.
    • Recruitment and modulation of additional inflammatory effector cells, such as macrophages
  • Clinical relevance:
    • Prominent role in intracellular pathogens (e.g., Listeria monocytogenes), as these pathogens spend little time in circulation (less susceptibility to antibodies).
    • Similar importance in the immune defense against viruses (e.g., HIV)

Other Types of T Cells

Gamma–delta T cells

  • TCRs consists of γ and δ chains.
  • Do not pass through double-positive stage, but have a distinct role complementary to that of αβ T cells
  • Represent < 5% of T cells 
  • Found in gut mucosa, skin, lungs, and uterus
  • Can bind to non-MHC molecules for activation
  • Recognize phosphoantigens from:
    • Mycobacterium tuberculosis
    • Plasmodium spp.

Natural killer (NK) T cells

  • Branch from T cells at the double-positive (CD4+, CD8+) stage of development.
  • Have morphologic and functional features of T cells and NK cells
  • Recognize antigen presented by MHC class I–like CD1d molecules
  • Produce both Th1 and Th2 cytokines when activated

Memory T cells

  • Can be either CD4+ or CD8+
  • Mount immune response years after initial exposure
  • Naive T cells not exposed to dendritic cells carrying antigens, express the following markers:
    • Positive for CD45RA
    • Negative for CD45RO
    • Express CD62L and CCR7
  • Following exposure to antigens, some T cells develop into memory cells:
    • Initially reside within lymphoid tissues (central memory T cells).
    • Become CD45RO+ and CD45RA–
    • CD62L+ and CCR7+
  • T memory cells that take residence in peripheral tissues (effector memory cells):
    • CD45RO+ and CD45RA–
    • CD62L– and CCR7–
  • Following reinfection by the same antigen, they become T effector cells:
    • CD45RA+, CD45RO–, CD62L–, and CCR7–
    • Essential components of secondary immunity.
    • Can be immediately activated upon pathogen invasion.
Memory T cells and expressed cellular markers

Memory T cells and expressed cellular markers:
The central memory T cells are in the lymphoid organs, while the peripheral memory T cells are in peripheral tissues.

Image by Lecturio. License: CC BY-NC-SA 4.0

Clinical Relevance

  • Chronic mucocutaneous candidiasis (CMCC): autoimmune syndrome with features that include chronic, noninvasive Candida infections of the skin, nails, and mucous membranes. The condition is associated with autoimmune manifestations (most commonly endocrinopathies). Hypoparathyroidism is the most common endocrine abnormality, occurring in 30% of individuals. Adrenal insufficiency occurs in > 60% of cases by the age of 15 years. CMCC is due to genetic defects in the immune system, including those affecting AIRE, signal transducer and activator of transcription 1 (STAT1), and the IL-17 pathway, among others.
  • IPEX (Immune dysregulation, Polyendocrinopathy, Enteropathy, X-linked) syndrome: caused by mutations in the gene for the transcription factor FOXP3. The defining feature of IPEX syndrome is regulatory T-cell impairment, manifesting as autoimmune disease with allergic inflammation. The syndrome typically presents in male infants with a triad of enteropathy, dermatitis, and autoimmune endocrinopathy (usually type 1 diabetes or thyroiditis). Diarrhea can be profound, associated with dehydration, malabsorption, metabolic acidosis, renal insufficiency, and failure to thrive. Other manifestations include severe food allergies, chronic autoimmune hepatitis, autoimmune cytopenias, interstitial nephritis, and developmental delays. Diagnosis is by mutational analysis of the FOXP3 gene. Hematopoietic cell transplantation is the only curative therapy available.
  • Adult T-cell leukemia/lymphoma: rare, but often aggressive mature T-cell malignancy caused by chronic infection of CD+ T cells with the human T-lymphotropic virus, type I (HTLV-I). The infection is endemic in Japan, the Caribbean region, and Central Africa. The general presentation is widespread involvement of lymph nodes, peripheral blood, and/or skin. Several clinical variants are known—acute, lymphomatous, chronic, and smoldering—and each has a different clinical course. The most characteristic features seen in the peripheral blood are “clover leaf” or “flower cells” (cells with bizarre hyperlobulated nuclei). Diagnosis is based on clinical presentation, morphologic and immunophenotypic changes of the malignant cells, and confirmed HTLV-I infection. The treatment is tailored to the subtype, and options include antiviral agents, monoclonal antibody therapy, chemotherapy and allogeneic stem-cell transplantation.

References

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