The so called sentinel cells are located in our skin to detect invasions by e.g. microbes and viruses in terms of the innate immune response. Macrophages and dendritic cells as well as mast cells belong to the class of antigen representing sentinel cells. When an infection is caused by invaders entering our tissue through a damaged epidermis (wound), the sentinel cells respond by releasing cytokines (there are about 50 different cytokines e.g. TNF and Interleukins [IL-1,IL-2, ... , IL-35]). Sentinel cells do not recognise molecules that allows them to classify specific cell types but rather broad classes of invaders such as for exapmle viruses or a bacterial cells (as opposed to the adaptive immune response that is more specific).
Cytokines cause vascular endothelial cells to produce adhesion molecules (E-selectin, P-selectin) and lead to vasodilation (widening of bood vessles). This results in extravasion of rolling leukocytes into the tissue and allows antibodies to enter the infection site. Chemokines presented by edothelial cells are specifically recognised by chemokine receptors of some leukocytes. Binding to the chemokine receptor activates extravasion, leukocytes bind to endothelial cells via ICAM-1/LFA-1 and then transmigrate into tissues. The recruited leukocytes then help to fight the infection. This process is known as inflammation and is accompanied by the cardianl signs: Dolor (pain), Calor (heat), Rubor (redness), Tumor (swelling), Functio laesa (loss of function).
The first leukocytes that fight infection are the neutrophiles. They are short-lived and have to be constantly produced by hematopoietic stem cells in the bown marrow. For infections lasting longer than a day, differnent chemokines are prouced, that attract another class of leukocytes known as monocytes.