" natural " child print: Too aggressive! The scientist discovers cancer cell first unexpectedly ca_News

Before before long, we just reported tumor can adopt system of the secrete outside releasing the T cell of long-range suppress whole body, cause airframe immunity ability to drop.

Recently, publish in top class periodical " natural medicine " the article that go up shows again, tumor still has more " demon unreal " the immune system of method attack human body [1] .

Peter E of American Du Ke university. Fecci teachs experimental group discovery of the leader, the tumour that enters cerebrum can make T cell cannot be come out in marrow by distrain. They confirm the cause that causes this one consequence is marrow of T cell discrepancy unexpectedly " visa " (accept put oneself in another's position of T cell surface) lost [1] !

This one research may be open up of auxiliary cancer medicaments a new exploration field, can release the T cell that is stranded from inside marrow, conduce to rise have the validity with new immune treatment.

Current, professor Peter group is in with lab of Robert Lefkowitz of nobel prize gainer cooperated 2012, development restores cellular surface to suffer the young member medicaments of body, release T cell from inside marrow, immunity of auxiliary T cell is treated [2] .

" natural " child print: Too aggressive! The scientist discovers cancer cell first unexpectedly can T cell " captivity " in marrow, science of so little ｜ discovers the T cell of patient of pardonable very much cancer greatly

Peter E. Fecci Robert Lefkowitz

Tumour of colloid mother cell (cancer of a kind of brain) the T lymphocyte that cause lacked disease to had perplexed a scientist 40 years [3] ! Professor Peter is the expert that studies cerebral cancer, the immune force of the patient of new diagnose of his research group discovery, tumour of colloid mother cell that has not accepted treatment is mixed unexpectedly AIDS patient is euqally low.

The amount of the cell of CD4 auxiliary T inside healthy human body is in 700-1000 (every microlitre) between even above, and patient of tumour of colloid mother cell has 200 only however fewer even. In the meantime, photograph of other T cell also has than normal person drop considerably. So low immunity result makes they get more easily all sorts of infection, bring about cancer aggravation possibly.

Milt is the immune organ with the largest human body, embedded and many lymphocyte. Because milt is hemal narrow, and the function that develops cleared blemish red blood cell, often appear injury [4] . Investigator people figure above all of T cell lienal segregation disease causes reduce a likelihood, can cause milt from this intumescent. Can study the result is as contrary as this however, video result shows the patient's milt has apparent atrophy.

For convenient research, compose built scientists model of small mouse of tumour of colloid mother cell. With human body likeness, small rat blood and lymphatic medium T cell also decreases considerably. Meanwhile, milt, thymus, cervical and lymphatic Jiedouming shows atrophy; Nevertheless, researcher is not clear that this is reason or result.

Where does the T cell of cancer patient go to after all? Be to form suffocate suffocate? Or " hide in " where?

Let us review the generation process of T cell. The hematopoiesis of marrow of T cell traceable does a cell, the course splits up step by step, become initiative T cell. Initiative T cell can transfer thymus, become mature T lymphocyte through treatment. The week outside be being released through thymus subsequently is lymphatic organization, enter human body blood and lymphatic circulatory system then, play immunity function [5] .

The migratory method of T cell

Then, scientists continue to begin a platoon to investigate the work.

Since appeared,the T cell of systematization decreases, did then T cell produce fountainhead to give an issue?

Then they checked the marrow that has small rat of tumour of colloid mother cell, the T cell amount in discovering small rat is medullary enlarged 3 - 5 times! The scientist returns discovery, other immunity cell did not increase, it is T cell increased merely.

This really unexpected, then, researcher tightens the medullary case that examined patient of tumour of colloid mother cell then, card is real in human body, t cell is rich in marrow also collect.

Original T cell is squeezed in marrow.

Scientists return will other tumour, if lung cancer of breast cancer, melanin tumour, Lewis and nerve are colloid,tumour transplants respectively small rat cranial cavity or hypodermic. Experimental result shows, all transplanting can cause T cell gather mediumly in marrow into the tumour inside skull, and hypodermic transplanting however won't.

This makes clear, cause T cell to be not the type with tumor in the reason of rich collect in marrow relevant, grow to be concerned where with tumor however. Look, the problem is very serious.

But are they waited for make in marrow very? Do not fight cancer for what?

To this phenomenon, researcher has such two guess: Or is marrow of flow direction of T cell apt, stay actively namely; Or they go out not to come from marrow at all.

Be which are planted after all? Researcher makes the T cell that collects from body of tumor small rat mark, inject respectively inside system of small mouse of tumor small rat and health, analyse again carefully, accident ground discovers: It is actually in T cell heart very resemble going to what front fights cancer, but they are to be stranded really go out not to go in marrow.

T is rich in marrow collect

And, researcher returns discovery, t cell is tired in marrow is not medullary play a dirty trick, however T cell oneself gave an issue.

Now, let us want to put the view on T cell body. T cell surface has a large number of structures of each different accept put oneself in another's position, it is to identify more among them sundry antigen and deliver signal to wait a moment. In the meantime, a gets body to still can serve as his status of T cell surface identifies, among them the proof that an action regards pass in and out as the organ namely.

Can you be T cell so is what the surface accepts put oneself in another's position some kind missing brought about its to cannot leave marrow? Eliminating a few kinds of likelihood hind with the experiment, researcher locks up the target what was in to call S1P1 surely to suffer on body. S1P1 is a G albumen idol couplet accepts put oneself in another's position [6] , already axis of S1P1 of reportorial S1P – can upright guide T cell leaves marrow [7] .

They figure the likelihood is the destruction that tumour of colloid mother cell brought about axis of S1P – S1P1, make T cell cannot leave marrow. That, we call S1P1 for the moment " visa " .

T cell surface accepts put oneself in another's position

Detect specially through a kind method, researcher discovers the S1P1 of T cell surface suffers system level to decrease greatly! This kind of surface accepts put oneself in another's position decrease to have intense dependency with the amount of cell of the T in marrow. Undertake knocking to small rat S1P1 divide or medicaments block is broken, also discovered T cell cannot leave marrow. These results make clear, it is T cell surface really " visa " be short of break bring about its to be locked up to be in marrow, cannot leave!

Nevertheless, in RNA level detect the expression of indication S1P1 does not have difference, the adjusting control of its upper reaches child also did not suffer an effect, and its are in cytoplasmic medium content also did not change. Not be S1P1 conveys a quantity to decrease it seems that cause, just be S1P1 cannot run to T cell surface, so researcher does not detect on cellular film S1P1.

But, it is what reason caused function of T cell S1P1 after all maladjusted, have what kind of immanent connection with the tumour that enters cerebrum again, still not be clear about at present. This is the work that should do after scientists.

Nevertheless, still let us return original issue first.

Since found the reason that is stranded,be " visa " missing, does that fill afresh on whether can visa obtain leave the country license?

There already was research to make clear before, the small rat that break is short of in GRK2 albumen function in, s1P1 accepts put oneself in another's position " interior is changed " can be restrained, s1P1 suffers experience to secure in T cell surface [8] . Then, investigator people the S1P1 gene that conveys too was knocked in mutation small rat, make the S1P1 of T cell surface suffers body to maintain the level that secures in.

Researcher confirms, after T cell surface restores S1P1 to accept put oneself in another's position, become can free pass in and out is medullary, and still can add the measure that cell of the activation inside small mouse system T takes! But the long-term survival rate that cannot raise tumor small rat however.

When researcher reoccupy 4-1BB excited nod block to break with the examination, when therapeutics of activation of cell of these two kinds of T treats tumor together, the long-term survival rate of the small rat that S1P1 of T cell surface gets body to secure rose 50% !

Long-term survival rate promotes tumor small rat

Because do not have medicaments to be able to secure S1P1 now,be in T cell surface, investigator people explored other method, will liberate by the T cell of captivity.

They discover market of the cell that use bead falls small rat of model of exciting factor processing, can make marrow releases T cell. Fall to exciting factor handles small rat and did not treat the effect with bead cell collect only, but couplet of as excited as 4-1BB agent is used make long-term survival rate promoted small rat nearly 40% ! This is meant, rescue by the T cell of medullary captivity, there is tremendous latent capacity in immune cure.

Scientists will continue to explore the tumour inside skull to cause S1P1 function maladjusted, cause T cell by the mechanism of captivity. At the appointed time, we will understand tumor to violate the pattern of immune system more, it is better to be found then answer way!

In the meantime, the scientist still develops surface of fixed T cell to suffer the young member medicaments of body in effort, make auxiliary immunity cure is moved toward as soon as possible clinical.

It is tumour of colloid mother cell not only, all cure that transfer the tumour inside the head are possible be benefited in this one research.

The battle of long be locked in a seesaw struggle of immune system and tumour develops today, it is tumor was occupied it seems that windward. But the affiliation that has scientist and doctor and collectivity mankind, human wisdom and mankind are driven civilizedly, we are turning a situation slowly, can gain last victory eventually!

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[1] Https://www.nature.com/articles/s415 91-018-0135-2

[2] Https://corporate.dukehealth.org/news-listing /duke-team-finds-missing-immune -cells-could-fight-lethal-brain-tumors

[3] Brooks, w. H. , roszman, t. L. , mahaley, m. S. &Woosley, r. E. Immunobiology Of Primary Intracranial Tumours. II. Analysis Of Lymphocyte Subpopulations In Patients With Primary Brain Tumours. Clin. Exp. Immunol. 29, 61 – 66 (1977)

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[7] Maeda, y. , seki, n. , sato, n. , sugahara, k. &Chiba, k. Sphingosine 1-phosphate Receptor Type 1 Regulates Egress Of Mature T Cells From Mouse Bone Marrow. Int. Immunol. 22, 515 – 525 (2010)

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