T Cells and Cell-Mediated Immunity

• Q1 — B: Cell-mediated immunity targets infected host cells using T lymphocytes; humoral immunity targets extracellular pathogens using antibodies from B cells. (A) reverses the definitions. (C) is wrong — both are adaptive. (D) is wrong — both operate in blood and tissues.
• Q2 — C: CTLs recognise viral peptides displayed on MHC class I — the TCR binds this specific complex. (A) describes NK cell detection — missing self, not foreign peptide recognition. (B) describes antibody function, not T cell recognition. (D) describes antibody-dependent cellular cytotoxicity — a different mechanism.
• Q3 — A: T helper cells provide cytokine signals (including IL-2 and CD40L co-stimulation) required for full B cell activation and CTL proliferation. (B) is wrong — T helper cells produce neither antibodies nor kill directly. (C) is wrong — MHC molecules are expressed by APCs and body cells, not T helper cells. (D) is partly correct (IL-2 activates CTLs) but incorrect about B cells — IL-2 drives T cell expansion; B cell activation requires a different set of T helper signals.
• Q4 — D: MHC class I displays intracellular peptides to CTLs. Without MHC class I, CTLs cannot recognise any infected cell, regardless of what is happening inside it — intracellular infections (viruses, some bacteria) cannot be cleared. (A) is wrong — B cell activation uses MHC class II on APCs. (B) is wrong — T helper cells recognise antigen on MHC class II, not MHC class I. (C) is wrong — absent MHC class I would trigger more NK cell killing, not less.
• Q5 — B: T helper cells coordinate both humoral and cell-mediated immunity — their loss impairs both simultaneously. B cells can produce some antibodies without T helper signals (T-independent antigens) but cannot mount a full IgG response (A is too absolute). CTLs can recognise infected cells via MHC class I regardless of T helpers — they just cannot be fully activated without IL-2 (C is wrong). The innate system continues to operate independently of T helper cells (D is wrong).

SA1: T helper cells carry the CD4 surface marker and are activated when their T cell receptor (TCR) binds antigen displayed on MHC class II molecules — found only on professional antigen-presenting cells (dendritic cells, macrophages, and B cells). Their function is coordination: they release cytokines (including IL-2, IL-4, and interferon-gamma) that activate B cells, stimulate CTL clonal expansion, enhance macrophage killing, and recruit innate cells. Crucially, T helper cells do not kill anything directly. Cytotoxic T cells (CTLs) carry the CD8 surface marker and are activated when their TCR binds viral or other foreign peptide displayed on MHC class I molecules — found on all nucleated body cells — combined with an IL-2 signal from a T helper cell. Their function is direct killing of infected cells: they release perforin (which inserts into the target cell membrane, forming pores) and granzymes (proteolytic enzymes that enter through the pores and activate apoptosis pathways in the target cell). The core distinction is coordinator versus effector killer — T helper cells direct the response; CTLs execute it.

SA2: When a cell is infected by a virus, the cell's own machinery processes viral proteins and loads viral peptide fragments onto MHC class I molecules, displaying them on the cell surface. Every nucleated cell in the body does this continuously — in a healthy cell, only self-peptides are displayed and ignored; in an infected cell, foreign viral peptides appear as a flag. A cytotoxic T cell (CD8+) with a TCR that matches that specific viral peptide-MHC class I complex binds to the infected cell. However, this recognition alone is not sufficient for full activation — the CTL also requires an IL-2 signal from an activated T helper cell that has independently recognised the same antigen. Once fully activated, the CTL undergoes clonal expansion, producing a clone army of identical killers. Each CTL kills its target by releasing perforin — a protein that inserts into the target cell membrane and polymerises to form pores — and granzymes — serine proteases that enter the target cell through the perforin pores and activate the caspase cascade, triggering apoptosis (programmed cell death). The infected cell dies from the inside, its contents packaged into apoptotic bodies rather than releasing viral particles into the surrounding tissue.

SA3: T helper cells (CD4+) are the central coordinators of the adaptive immune response, providing essential signals to both the humoral and cell-mediated arms. In humoral immunity, activated T helper cells provide a co-stimulatory signal (via CD40L binding to CD40 on B cells, plus cytokines such as IL-4 and IL-21) that is required for full B cell activation, clonal expansion, and antibody class switching from IgM to IgG — the high-affinity antibody that provides long-term protection. Without this T helper signal, B cells produce only weak, short-lived IgM responses and cannot form effective memory. In cell-mediated immunity, T helper cells release IL-2 and other cytokines that drive clonal expansion of cytotoxic T cells — without IL-2, CTLs cannot proliferate into the large clone army needed to clear an infection. HIV targets CD4+ T helper cells specifically because the viral surface protein gp120 binds to the CD4 receptor. As the CD4+ count progressively falls, both arms of adaptive immunity are simultaneously starved of coordination signals. The antibody response weakens — B cells exist but cannot be fully activated for high-affinity IgG production. The CTL response weakens — existing CTLs cannot expand adequately to clear infections. The clinical consequence is susceptibility to opportunistic pathogens — organisms like Pneumocystis jirovecii, Toxoplasma gondii, and Cryptococcus neoformans — that a healthy immune system eliminates routinely but that become life-threatening when T helper coordination is lost.