Immunological Memory 면역학적 기억

Immunological memory에 대하여 생각해본다.

Vaccine의 존재이유는 이 memory를 증강시키기 위함이다. smallpox와 polio의 효과적인 예방은 이러한 memory의 극적인 이용에서 비롯된다.

그럼에도 불구하고 Jenner와 Pasteur이후로 백신의 개발은 완전한 이해를 기반으로 하는 정교한 작업이 아닌 'hit-or-miss' affair(때려맞추기)와 같았다.

http://www.nature.com/ni/focus/immunologicalmemory/

이번달의 Nature Immunology에서 Focus로 면역학적 기억에 대해서 다루고 있다.

T cell과 B cell memory와 immune exhaustion, physical compartmentalization of memory, 새로운 백신의 개발과 NK cell memory등에 대해 다루고 있다.

PDF: http://www.nature.com/ni/journal/v12/n6/pdf/ni0611-461.pdf

B cell의 memory에 대한 개략적인 그림

Crotty & Ahmid, 2004 Seminars in Immunology

http://www.liai.org/files/Memory-Crotty.pdf

Fig. 1. Memory B cell and plasma cell differentiation. Following antigenic
stimulation, na¨ıve B cells undergo clonal expansion and form clusters of
activated B cells known as extrafollicular foci. These activated B cells can
either differentiate into short-lived plasma cells, or they can migrate back
into the follicle and initiate a germinal center reaction. After proliferation
and affinity maturation, germinal center B cells produce both long-lived
plasma cells that produce high affinity antibodies and memory B cells that
have high affinity B cell receptors. Memory B cells presumably self-renew
by homeostatic proliferation. Memory B cells may also periodically differentiate,
in an antigen-dependent or antigen-independent manner, into
long-lived plasma cells to maintain long-term antibody production.

Lymphoproliferative Disorders에 대해 총정리

http://www6.ufrgs.br/favet/imunovet/molecular_immunology/pathohomotissueblood_WBCneoplasm.html

좋은 글.

Lymphoproliferative Disorders에 대해 총정리한 글.

Mechanism of monocyte migration

Chemokine-driven migration of monocytes and DC progenitors.

In mice, two populations of circulating monocytes exist: resident monocytes (Mac1⁺Gr1^-F4/80⁺CX₃CR1^hi) and inflammatory monocytes (Mac1⁺Gr1⁺F4/80⁺CX₃CR1^midCCR2⁺). In the absence of an inflammatory stimulus, CX₃C-chemokine ligand 1 (CX₃CL1; also known as fractalkine) and CC-chemokine ligand 3 (CCL3; also known as macrophage inflammatory protein 1, Mip1) preferentially induce the recruitment of resident monocytes into tissues, whereas CCL2 (also known as monocyte chemotactic protein 1, Mcp1) recruits inflammatory monocytes to inflamed tissue. By contrast, dendritic cell (DC) precursors can be recruited directly from the blood to the lymphoid organs, through signalling induced by CC-chemokine receptor 5 (CCR5)–CCL3 interactions. Direct recruitment of inflammatory monocytes to lymph nodes can occur through high endothelial venules (HEVs) and is mediated by CXC-chemokine ligand 9 (CXCL9; also known as monokine induced by interferon-, Mig). After migration to the peripheral tissue, activated inflammatory monocytes can differentiate into DCs and gain access to the draining lymph nodes through the lymphatics. Inflammation leads to upregulation of CCL21 expression by the lymphatics and upregulation of CCR7 by antigen-presenting cells. Activated resident DCs or newly recruited granulocytes can produce factors that inhibit these differentiation pathways and routes of migration. CX₃CR1, CX₃C-chemokine receptor 1.