Aktivasi sel T

Antigen recognition by a TCR with CD4 or CD8 proteins is the first signal in activation
of a T cell.
A T cell becomes activated only if it binds to the foreign antigen
and at the same time receives a second signal, a process known as costimulation. Of the more than 20
known costimulators, some are cytokines, such as interleukin-2. Other costimulators include pairs of
plasma membrane molecules, one on the surface of the T cell and a second on the surface of an
antigen-presenting cell, that enable the two cells to adhere to one another for a period of time.
Aktivasi neutrofil
Fungsi: Tissue remodeling
Direct harm to pathogens
Regulation of proteases
Vasodilation, infl ammation

Phagocytosis. Destruction of bacteria with lysozyme, defensins, and strong oxidants, such as
superoxide anion, hydrogen peroxide, and hypochlorite anion.
Fungsi eosinofil:
Induces formation of ROS
Vasodilation, basophil degranulation
Antiviral activity
Modulation of adaptive immune responses

Combat the effects of histamine in allergic reactions, phagocytize antigenantibody

complexes, and destroy certain parasitic worms.
Fungsi basofil
Liberate heparin, histamine, and serotonin in allergic reactions that intensify the overall
inflammatory response.
Fungsi sel mast
mast cells release substances involved in inflammation, including heparin, histamine, and
proteases.
Modulation of adaptive immune response
Regulation of inflammation
Vasodilation, smooth muscle activation

The principal functions of B cells are to make antibodies against antigens, to perform
the role of antigen-presenting cells (APCs), and to develop into memory B cells after
activation by antigen interaction.
Eosinophils develop and mature in the bone marrow. They differentiate from myeloid precursor
cells in response to the cytokines interleukin 3 (IL-3), interleukin 5 (IL-5), andgranulocyte
macrophage-colony stimulating factor (GM-CSF).
After maturation, eosinophils circulate in blood and migrate to inflammatory sites in tissues, or to
sites of helminth infection in response to chemokines like CCL11 (eotaxin-1), CCL24 (eotaxin-2),
CCL5 (RANTES), and certain leukotrienes like leukotriene B4 (LTB4) and MCP1/4. At these
infectious sites, eosinophils are activated by Type 2 cytokines released from a specific subset
of helper T cells (Th2); IL-5, GM-CSF, and IL-3 are important for eosinophil activation as well as
maturation.

Aggregation of FcR1 by polyvalent antigen recognized by bound IgE activates mast

cells and is the basis for anaphylaxis and other allergic diseases. FcR1 density on the
surface of mast cells is upregulated in the presence of elevated free IgE levels and in the
presence of IL-4, thus enhancing activation. In addition, mast cells are activated by C3a

and C5a through C3aR and C5aR (CD88), nerve growth factor through TRKA, and
IgG through FcR1. Mast cells are also activated by TLR ligands. For example,
activation through TLR3 by double-stranded RNA induces human mast cells to
produce interferon-. The extent and pattern of mediators released depends on the signal, its
intensity, and the cytokine milieu. Mediator release, for example, is enhanced in the presence
of SCF.6, 7
Eosinophils can be activated by cross-linking of IgG or IgA Fc receptors by agarose beads
with IgG, IgA, or secretory IgA, with the latter being most potent. Eosinophils can be primed
for activation by a number of mediators, including IL-3, IL-5, GM-CSF, CC chemokines, and
platelet-activating factor. The outcome of activation is variable, with four mechanisms of
eosinophil degranulation reported: exocytosis, compound exocytosis, piecemeal exocytosis,
and cytolysis. Different mediators of activation may differentially affect the type of
degranulation and factors expressed in the activated state.
Basophils express a complete FcRI (2), the surface expression of which directly
correlates with free IgE concentration. Aggregation of FcRI bound to IgE by multivalent
antigen leads to basophil activation, granule exocytosis, and mediator release. C3a and C5a
also activate basophils through their receptors on the surface of basophils. IL-3, IL-5, GMCSF, histamine releasing factor (HRF), as well as several chemokines, prime basophils
leading to enhanced degranulation and IL-4 and IL-13 secretion following FcRI activation,
but do not fully activate basophils alone.3
Monocytes and their macrophage and dendritic-cell progeny serve three main functions in the
immune system. These are phagocytosis, antigen presentation, and cytokine
production. Phagocytosis is the process of uptake of microbes and particles followed by digestion
and destruction of this material. Monocytes can perform phagocytosis using intermediary
(opsonising) proteins such as antibodies or complement that coat the pathogen, as well as by
binding to the microbe directly via pattern-recognition receptors that recognize pathogens.
Monocytes are also capable of killing infected host cells via antibody-dependent cell-mediated
cytotoxicity. Vacuolization may be present in a cell that has recently phagocytized foreign matter.

In spite of a spectrum of ways to activate macrophages, there are two

main groups designated M1 and M2. M1 macrophages, as mentioned
earlier (previously referred to as classically or alternatively activated
macrophages), M1 "killer" macrophages are activated by LPS and IFNgamma, and secrete high levels of IL-12 and low levels of IL-10. In
contrast, the M2 "repair" designation broadly refers to macrophages that
function in constructive processes like wound healing and tissue repair,
and those that turn off damaging immune system activation by producing
anti-inflammatory cytokines like IL-10. M2 is the phenotype of resident
tissue macrophages, and can be further elevated by IL-4. M2
macrophages produce high levels of IL-10, TGF-beta and low levels of
IL-12. Tumor-associated macrophages are mainly of the M2 phenotype,
and seem to actively promote tumor growth.
Aktivasi makrofag diakibatkan adanya peningkatan transkripsi gen-gen. Karena
adanya peningkatan ekspresi gen-gen tersebut maka makrofag dapat melakukan
fungsi yang tidak dapat dilakukan oleh sel yang sama dalam keadaan istirahat.
Fungsi tersebut antara lain adalah killing bakteria yang sudah difagositosis. Sitokin
aktivator makrofag yang poten adalah IFN-g. IFN-g bukanlah satu-satunya sitokin

yang mengaktivasi makrofag, tetapi makrofag juga diaktivkan oleh kontak dengan
limfosit T melalui CD 40.

Aktivasi makrofag diakibatkan adanya peningkatan transkripsi gen-gen dimana sitokin

aktivator makrofag yang poten adalah IFN-gamma. IFN-gamma bukanlah satu-satunya
sitokin yang mengaktivasi makrofag, tetapi makrofag juga diaktifkan oleh kontak dengan
limfosit T melalui CD 40.
B cell activation requires both antigen engagement by the B-cell receptor (BCR) and direct contact
with an activated CD4_ TH cell. Both events are facilitated by the anatomy of the lymph node. Like T
cells, B cells circulate through the blood and lymph and visit the lymph nodes on a daily basis,
entering via the HEV. They respond to specific signals and chemokines that draw them not to the
paracortex but to the lymph node follicle. Although they may initially take advantage of the FRCC for
guidance, they ultimately depend upon follicular dendritic cells (FDCs) for guidance (Figure 2-9c).
FDCs are centrally important in maintaining follicular and germinal center structure and presenting
antigen to differentiating B cells.
B cells differ from T cells in that their receptors can recognize free antigen. A B cell will typically meet
its antigen in the follicle. If its BCR binds to antigen, the B cell becomes partially activated and engulfs
and processes that antigen. As mentioned above, B cells, in fact, are specialized antigen-presenting
cells that present processed peptide- MHC complexes on their surface to CD4_ TH cells. Recent
data show that B cells that have successfully engaged and processed antigen change their migration
patterns and move to the T-cell-rich paracortex, where they increase their chances of encountering an
activated CD4_ TH cell that will recognize the MHC-antigen complex they present.
When they successfully engage this TH cell, they maintain contact for a number of hours, becoming
fully activated and receiving signals that induce B cell proliferation (see Chapter 14).
Some activated B cells diff erentiate directly into an antibody- producing cell (plasma cell) but others
re-enter the follicle to establish a germinal center. A follicle that develops a germinal center is
sometimes referred to as a secondary follicle; a follicle without a germinal center is sometimes
referred to as a primary follicle.