Treatment that interferes with inhibitory immune regulatory interactions, such as PD-1/PD-L1 or CTLA-4-associated restraint. It requires a usable antitumour recognition and effector system.

Transfer of prepared T cells to a patient to supply or amplify a therapeutic immune response, including expanded tumour-derived or genetically engineered populations.

An intervention intended to generate or strengthen immune recognition of tumour-associated targets. Successful priming does not guarantee entry or function within a tumour.

Human leukocyte antigen, the human MHC system. Particular HLA molecules restrict which peptides a conventional T-cell receptor can recognise.

An altered T-cell functional and regulatory state associated with persistent stimulation. Blocking one inhibitory receptor need not reverse every component of the state.

A major histocompatibility complex presentation system displaying intracellularly derived peptides to appropriate T cells. Presentation and direct CAR recognition have different requirements.

An antigen-presentation system displaying peptides to appropriate CD4 T cells. Its usual source and processing route differ from the intracellular-protein sampling pathway of MHC class I.

Collective protection against pathogens arising through interactions among individuals, including hygienic behaviour. A colony-level reduction in infection need not be increased cellular immunity in every worker.

Study of interactions among animal behaviour, the nervous system and immunity. Bidirectional mechanisms require interventions or temporal evidence beyond a cross-sectional association.

Reduction of pathogen burden through prevention or control of infection. It differs from disease tolerance, which reduces damage at a given burden.

Reduction of health or fitness damage for a given pathogen burden. Low symptoms alone cannot distinguish tolerance from successful disease resistance.

Experimental manipulation intended to stimulate an immune response. A nonreplicating inflammatory stimulus separates some host responses from effects of a live pathogen, but need not reproduce natural infection.

A coordinated tissue response involving immune activity, vascular changes and cellular signaling after injury or challenge. It can support defense and repair while also causing damage when excessive or persistent.

Immune responses involving antigen-specific lymphocyte recognition and the capacity for memory. Expansion of selected cell populations connects molecular specificity with a changed response on later exposure.

Immune defense using pre-existing recognition and response mechanisms, including barriers and rapid cellular reactions. It is distinguished from antigen-specific adaptive responses without implying that its behavior is identical in every prior exposure state.

Cellular and molecular changes following recognition of a challenge. Increased activation can reflect increased exposure or damage, so its magnitude is not interchangeable with protective capacity.

A host with sufficiently functional immune defenses for the specified comparison. Competence is contextual rather than a guarantee of resistance to every infection or an absence of immune variation.

An imine whose imine carbon bears two carbon substituents. Hydrolysis passes through a carbinolamine and gives a ketone.

Cell segmentation assigns image pixels or voxels to individual cells or their regions. It can distinguish foreground from background, separate touching cells, and label each object for later measurements. For example, a fluorescent nuclear image can support counting nuclei, but nuclear boundaries need not coincide with whole-cell boundaries. Thresholding, geometric models and learned methods make different assumptions about contrast and shape. Errors such as merging two cells or splitting one cell can bias counts and size distributions, so evaluation must match the biological quantity being measured.

For the real line at radius $b>a$ and polar angle measured toward it, the exterior radial field gives $\sigma (\theta )=-\lambda (b^2-a^2)/[2\pi a(b^2+a^2-2ab\cos \theta )]$. Its integral around the circumference is $-\lambda$ per unit axial length. At $b=2a$, this becomes $-3\lambda /[2\pi a(5-4\cos \theta )]$. The nearer surface has larger induced charge magnitude.