anergic

These B cells are said to be anergic.

Anergic cells will not respond to any antigen in the future, even if both signals are present later on.

Instead, they could avert an attack simply by tricking cells into entering the anergic state.

Lymphocytes are said to be anergic when they fail to respond to their specific antigen.

Tranylcypromine is highly effective in the treatment of anergic depression in comparison to placebo.

If T-lymphocyte does not receive costimulatory signal, its activation fails and it becomes anergic.

This results in the cell becoming anergic (anergy is generated from the unprotected biochemical changes of Signal 1).

If the initial inflammation is survived, the host cells become anergic or are deleted, resulting in a severely compromised immune system.

Usually, self reactive B cells remain anergic in the periphery without T cell co-stimulation.

Without it, the T cell becomes anergic, and it becomes more difficult for it to activate in future.

In comparison to imipramine, tranylcypromine has been shown to be more effective in anergic bipolar depression, and results in fewer patients leaving treatment.

Comparison of the clinical status of responder versus anergic patients showed no correlation with previous viral or bacterial opportunistic infections.

Unlike conventional T cells, regulatory T cells do not produce IL-2 and are therefore anergic at baseline.

It increases dopamine and norepinephrine levels and has stimulating effects, hence it is useful for anergic and apathetic depressives.

If mature B cells recognize soluble antigen in the periphery in the absence of T cell help, they lose surface IgM receptors and become anergic.

(2003) GRAIL: A novel E3 ubiquitin ligase that inhibits cytokine gene transcription is expressed in anergic CD4+ T cells.

Although such findings suggest that synovial T cells might be partly anergic, more recent studies have indicated that the T cells found in the RA synovium were postactivated cells.

Association of the TCR of a naive T cell with MHC:antigen complex without CD28:B7 interaction results in a T cell that is anergic.

Through IL-10, adenosine and other molecules secreted by regulatory T cells, the CD8 cells can be inactivated to an anergic state, which prevent autoimmune diseases such as experimental autoimmune encephalomyelitis.

Norepinephrine Reuptake Inhibitors (NRIs) like reboxetine may be especially useful in drive-deficient "anergic" states where the capacity for sustained motivation is lacking; and for melancholic depressives with a poor ability to cope with stress.

For example, NFAT and MAPK/ERK kinase pathways are expressed in anergic (or "tolerant) cell lines, whereas NF-kB and c-Jun N-terminal kinases pathways are not.

In induced models of autoimmunity, the CD28-B7 interaction has been shown to regulate disease susceptibility by rendering autoreactive T cells anergic, or alternatively by upregulating the threshold for autoreactive T-cell activation [ 30 ] .

Activation of a significant fraction of CD4 cells by a superantigen would greatly increase the number of cells susceptible to virus infection and replication and, at the anergic phase, allow provirus to remain latent in some of these cells.

In another experiment, Watson and Lee discovered that memory T-cells created by normal antigen stimulation were anergic to SAg stimulation and that memory T-cells created after a SAg infection were anergic to all antigen stimulation.