Fig. 2 | Mucosal Immunology

Fig. 2

From: Antigen-specific regulatory T-cell responses against aeroantigens and their role in allergy

Fig. 2

Two alternative models for uptake of aeroantigens and induction of protective and pathogenic T-cell responses: a classical model: allergenic proteins are rapidly released from inhaled particles and thus have preferential access to the immune system, e.g., their small size and protease activity facilitate transfer across the epithelial barrier, uptake by antigen-presenting cells (APCs), and activation of T cells. They either induce tolerance (Tr1 and Treg) or protective Th1 responses in healthy donors vs. Th2 responses in allergic donors. b New model: particle-associated proteins represent the immmunodominant antigens generating preferentially Treg responses that suppress the activation of naive Tcons. Thus, particles may cross the epithelial barrier and can be taken up by APCs. A single particle contains enough antigen to generate a T-cell responses. Bystander suppression protects all particle-associated antigens that are taken up (group tolerance). In contrast, soluble antigens are released before particle uptake and due to their extremely low dose cannot be efficiently taken up by APCs and fail to induce Treg or Tcon responses in healthy donors (ignorance). Under conditions favoring Th2 development, such as the genetic background, environmental factors, antigen dose, or a different APC type only those soluble antigens not protected by specific Tregs represent potential Th2 targets. T-cell priming typically occurs in the draining lymph node rather than in the mucosal tissue. However, where and by which APCs the antigens are taken up and are presented is currently not clear

Back to article page