Immunity: releasing killer proteins (Introduction)

by David Turell , Tuesday, November 28, 2017, 18:41 (2553 days ago) @ David Turell

We have several levels of immunity, innate, from colostrum, and learned, and aat some levels requiring injections of killer proteins:

https://medicalxpress.com/news/2017-11-cells-il-decades.html

" Researchers at Boston Children's Hospital have identified, for the first time, the molecule that enables immune cells to release interleukin-1 (IL-1), a key part of our innate immune response to infections. Findings were published online today by the journal Immunity.

"IL-1, first described in 1984, is the original, highly potent member of a large family of cellular signaling molecules called cytokines, which regulate immune responses and inflammation.

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"Most proteins have a secretion signal that causes them to leave the cell," says Jonathan Kagan, PhD, an immunology researcher in Boston Children's Hospital's Division of Gastroenterology and senior author of the new study. "IL-1 doesn't have that signal.

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"Recent work elsewhere at Boston Children's, for example, demonstrated that a protein called gasdermin D punches holes in the membranes of infected cells by forming pores. This releases IL-1 and other cytokines—but it also kills the cell, through an inflammatory cell-death program called pyroptosis.

"In the new study, Kagan and first author Charles Evavold showed that gasdermin D also enables the release of IL-1 from living immune cells.

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"Last year, Kagan, Ivan Zanoni, PhD, and colleagues reported in Science that IL-1 can be released from living dendritic cells, immune cells that present antigens to T cells. They showed that dendritic cells can enter a hyperactivated state in which they secrete IL-1, boosting their ability to rally memory T cells. But the question of how IL-1 gets released remained unanswered.

"The new study involved hyperactivated macrophages, immune cells that engulf and ingest pathogens. "We found, in hyperactivated cells, that gasdermin forms enough pores to let IL-1 pass through, but not enough to kill the cell," says Kagan.

"The immune response is like a yin-yang: If it's too weak, you're susceptible to infections; if it's too strong, the system can tip toward autoimmune disease and, in the face of a serious infection, sepsis.

"Gasdermin D inhibition is under study as a way of curbing inflammation-related diseases and sepsis. But Kagan's team is looking at the flip side, exploring gasdermin D as a target for stimulating IL-1 release from living, working cells to make vaccines more potent and long-lasting."

Comment: Note that this research is looking at killer proteins which are produced by cells that are protected from its effects. Only design can produce this. Chance evolution cannot form a cell that supplies lethal poison without supplying a protection for that cell at the same time. That is two coordinated steps (mutations) simultaneously.