## Was ist Thymosin Alpha-1?
Thymosin Alpha-1 (T\u03b11, INN: Thymalfasin) ist ein nat\u00fcrlich vorkommendes, N-terminal acetyliertes Peptid aus 28 Aminos\u00e4uren, das urspr\u00fcnglich aus Thymosin-Fraktion 5 isoliert und in PNAS vollst\u00e4ndig sequenziert wurde [Goldstein 1977]. Es wird \u00fcblicherweise als der N-terminale Abschnitt des Vorl\u00e4uferproteins Prothymosin alpha (ProT\u03b1) beschrieben. Pharmakologisch ist T\u03b11 als immunmodulatorisches Peptid charakterisiert, das auf der Ebene dendritischer Zellen \u00fcber Toll-like-Rezeptoren und den MyD88-Signalweg wirkt [Romani 2004; King & Tuthill 2016]. Die Sequenz ist Ac-SDAAVDTSSEITTKDLKEKKEVVEEAEN (28 aa, N-terminal acetyliert). Reborn Peptides liefert Thymosin Alpha-1 ausschlie\u00dflich als Laborforschungs-Compound.<\/p>\n
## Research-Profil
Kurz gesagt: Die Studienlage positioniert Thymosin Alpha-1 als eines der am breitesten dokumentierten immunmodulatorischen Forschungspeptide \u00fcberhaupt. In Studien wurde T\u03b11 im Zusammenhang mit folgenden Forschungsmarkern untersucht:
– TLR\/MyD88-Signalgebung in dendritischen Zellen \u2014 DC-Reifung und IL-12-Produktion \u00fcber den p38-MAPK\/NF-\u03baB-Weg, MyD88-abh\u00e4ngig \u00fcber distinkte Toll-like-Rezeptoren [Romani 2004; King & Tuthill 2016];
– TLR9\/MyD88\/IRF7 \u2192 Interferon (IFN-\u03b1\/IFN-\u03b3) \u2014 Aktivierung plasmazytoider dendritischer Zellen [Bozza 2007];
– Entz\u00fcndungs-\/Toleranz-Balance \u2014 TLR9 \u2192 IDO\/Tryptophan-Katabolismus, IL-10 und regulatorische T-Zellen [Romani 2006; Romani 2007];
– T-Zell-Reifung \u2014 Bildung funktioneller Helfer-T-Zellen [Low 1979];
– NK-Zell-Aktivit\u00e4t \u2014 als eines der untersuchten Thymus-Faktoren [Bistoni 1984];
– Humane Immunfunktions-Forschung \u2014 Monozyten-HLA-DR (RCT) sowie zirkulierende T-Zell-Zahlen und T-Zell-Ersch\u00f6pfungsmarker (PD-1\/Tim-3) [Wu 2013; Liu 2020].<\/p>\n
## Struktur & Identifikatoren
– Name \/ Synonyme: Thymosin Alpha-1 \/ T\u03b11 \/ Thymalfasin \/ \u03b11-Thymosin
– Klasse: nat\u00fcrlich vorkommendes, N-acetyliertes 28-aa-Thymuspeptid; immunmodulatorisches Peptid (TLR\/MyD88-Signalgebung in dendritischen Zellen)
– Ursprung: isoliert aus Thymosin-Fraktion 5; N-terminaler Abschnitt von Prothymosin alpha (ProT\u03b1) \u2014 als Hintergrund, vor harter Aussage best\u00e4tigen
– Sequenz: Ac-SDAAVDTSSEITTKDLKEKKEVVEEAEN (28 aa, N-terminal acetyliert) \u2014 per batch analytics best\u00e4tigen
– CAS: 62304-98-7
– PubChem CID: 16130571
– Summenformel: C129H215N33O55
– Molgewicht: ca. 3108.3 g\/mol (Durchschnitt) \u2014 exakte Masse\/Salzform per batch analytics best\u00e4tigen
– InChIKey: NZVYCXVTEHPMHE-ZSUJOUNUSA-N
– Regulatorischer Status (neutraler Kontext): bekanntes Thymuspeptid; in einigen L\u00e4ndern als Thymalfasin\/Zadaxin vermarktet; nicht FDA\/EMA-zugelassen; bei EU-Research-Peptid-Anbietern erh\u00e4ltlich. Reborn positioniert strikt Research Use Only.<\/p>\n
## Research Overview
In Studien wurde gezeigt, dass Thymosin Alpha-1 Effekte auf folgende Forschungsbereiche haben kann: Toll-like-Rezeptor-\/MyD88-Signalgebung in dendritischen Zellen, Th1-Zytokin-Polarisierung, T-Zell- und NK-Zell-Forschungsmarker sowie die Balance aus Entz\u00fcndung und Toleranz. Mechanistisch wurde in pr\u00e4klinischen Modellen gezeigt, dass T\u03b11 die funktionelle Reifung dendritischer Zellen und die IL-12-Produktion induziert \u2014 \u00fcber den p38-MAPK\/NF-\u03baB-Weg und MyD88-abh\u00e4ngig \u00fcber distinkte Toll-like-Rezeptoren \u2014 und in vivo eine Th1-gerichtete Immunantwort anst\u00f6\u00dft [Romani 2004]. \u00dcber TLR9\/MyD88\/IRF7 aktiviert T\u03b11 plasmazytoide dendritische Zellen und den IFN-\u03b1\/IFN-\u03b3-Effektorweg [Bozza 2007]. Bemerkenswert ist die regulatorische Seite: \u00dcber TLR9 und den Typ-I-Interferon-Rezeptor aktiviert T\u03b11 den IDO\/Tryptophan-Katabolismus, was mit IL-10-Produktion und der Bildung regulatorischer T-Zellen einhergeht \u2014 also einer Balance aus Entz\u00fcndung und Toleranz, nicht blo\u00df einer einseitigen Aktivierung [Romani 2006]. Diese mechanistische Tiefe ist der zentrale, am besten belegte und compliance-seitig sicherste Forschungsanker des Molek\u00fcls.
Die zellul\u00e4re Breite ist ungew\u00f6hnlich gut dokumentiert: T\u03b11 wurde im Zusammenhang mit der Reifung funktioneller Helfer-T-Zellen [Low 1979], mit direkter Wirkung auf dendritische Zellen [Huang 2004] und mit NK-Zell-Aktivit\u00e4t [Bistoni 1984] untersucht. \u00dcbersichtsarbeiten positionieren T\u03b11 als endogenen Regulator von Entz\u00fcndung, Immunit\u00e4t und Toleranz mit pleiotroper, TLR-\/dendritisch-zell-vermittelter Wirkung [Romani 2007; King & Tuthill 2016]. In der humanen Immunfunktions-Forschung wurde T\u03b11 in einer randomisierten kontrollierten Studie im Zusammenhang mit dem Monozyten-HLA-DR-Marker [Wu 2013] sowie in retrospektiver Forschung im Zusammenhang mit zirkulierenden T-Zell-Zahlen und T-Zell-Ersch\u00f6pfungsmarkern (PD-1\/Tim-3) [Liu 2020] untersucht \u2014 als Forschungs-Endpunkte, nicht als Produktwirkung.<\/p>\n
## Evidence Highlights
– PNAS 1977 (Goldstein et al.): Thymosin Alpha-1 als sequenzdefiniertes 28-aa-N-acetyliertes Thymuspeptid isoliert und charakterisiert.
– Blood 2004 (Romani et al.): T\u03b11 aktiviert dendritische Zellen \u00fcber TLR\/MyD88\/NF-\u03baB mit IL-12-Produktion und Th1-Polarisierung.
– Int Immunol 2007 (Bozza et al.): T\u03b11 aktiviert plasmazytoide DCs \u00fcber TLR9\/MyD88\/IRF7 und den IFN-\u03b1\/IFN-\u03b3-Weg.
– Blood 2006 (Romani et al.): T\u03b11 engagiert eine IDO\/IL-10\/Treg-Achse \u2014 Balance aus Entz\u00fcndung und Toleranz.
– Crit Care 2013 \/ Clin Infect Dis 2020 (Wu et al. \/ Liu et al.): humane Immunfunktions-Forschung zu Monozyten-HLA-DR bzw. T-Zell-Zahlen und Ersch\u00f6pfungsmarkern (modellqualifiziert).<\/p>\n
Die folgenden Quellen st\u00fctzen die auf dieser Produktseite verwendeten, study-framed Research-Claims. Alle Aussagen bleiben modell-\/studienbezogen und ersetzen keine medizinische Aussage.<\/p>\n
Quelle:<\/strong> Goldstein AL, Low TL, McAdoo M, McClure J, Thurman GB, Rossio J, Lai CY, Chang D, Wang SS, Harvey C, Ramel AH, Meienhofer J, 1977, Proceedings of the National Academy of Sciences USA<\/p>\n Research Area:<\/strong> Compound identity; isolation and primary-sequence analysis of an immunologically active thymic polypeptide<\/p>\n Finding:<\/strong> Thymosin alpha 1 was isolated from thymosin fraction 5 and characterized as a highly acidic 28-amino-acid, N-terminally acetylated polypeptide; the study reported its complete amino-acid sequence and confirmed it as an immunologically active thymic peptide.<\/p>\n Website Claim:<\/strong> Thymosin alpha 1 has been characterized as a naturally occurring, sequence-defined 28-amino-acid N-acetylated thymic peptide.<\/p>\n DOI: 10.1073\/pnas.74.2.725 \u00b7 PMID: 265536 \u00b7 URL: https:\/\/pubmed.ncbi.nlm.nih.gov\/265536\/<\/p>\n Quelle:<\/strong> Low TL, Thurman GB, Chincarini C, McClure JE, Marshall GD, Hu SK, Goldstein AL, 1979, Annals of the New York Academy of Sciences<\/p>\n Research Area:<\/strong> T-cell maturation\/differentiation; thymosin alpha 1 within a family of thymic factors controlling T-cell maturation<\/p>\n Finding:<\/strong> Within a family of purified thymic peptides acting at distinct steps of T-cell maturation, thymosin alpha 1 induced the formation of functional helper T-cells and the conversion of Lyt-negative cells to Lyt-1+,2+,3+ cells, supporting a role for T\u03b11 in inducing\/maintaining T-cell function.<\/p>\n Website Claim:<\/strong> In preclinical research, thymosin alpha 1 has been studied in relation to T-cell maturation and the formation of functional helper T-cells.<\/p>\n DOI: 10.1111\/j.1749-6632.1979.tb47095.x \u00b7 PMID: 394636 \u00b7 URL: https:\/\/pubmed.ncbi.nlm.nih.gov\/394636\/<\/p>\n Quelle:<\/strong> Romani L, Bistoni F, Gaziano R, Bozza S, Montagnoli C, Perruccio K, Pitzurra L, Bellocchio S, Velardi A, Rasi G, Di Francesco P, Garaci E, 2004, Blood<\/p>\n Research Area:<\/strong> Dendritic-cell maturation; Toll-like receptor \/ MyD88 \/ NF-\u03baB signalling; IL-12; Th1 polarization<\/p>\n Finding:<\/strong> Thymosin alpha 1 induced functional maturation and IL-12 production by fungus-pulsed dendritic cells through the p38 MAPK \/ NF-\u03baB pathway, signalling via the MyD88-dependent pathway involving distinct Toll-like receptors. In vivo, the synthetic peptide activated Th1-dependent antifungal immunity, accelerated myeloid-cell recovery, and protected transplant-recipient mice from aspergillosis.<\/p>\n Website Claim:<\/strong> In preclinical models, thymosin alpha 1 has been shown to activate dendritic cells via Toll-like receptor \/ MyD88 \/ NF-\u03baB signalling, with IL-12 production and Th1 polarization.<\/p>\n DOI: 10.1182\/blood-2003-11-4036 \u00b7 PMID: 14982877 \u00b7 URL: https:\/\/pubmed.ncbi.nlm.nih.gov\/14982877\/<\/p>\n Quelle:<\/strong> Romani L, Bistoni F, Perruccio K, Montagnoli C, Gaziano R, Bozza S, Bonifazi P, Bistoni G, Rasi G, Velardi A, Fallarino F, Garaci E, Puccetti P, 2006, Blood<\/p>\n Research Area:<\/strong> Inflammation\u2013tolerance balance; TLR9 signalling; indoleamine 2,3-dioxygenase (IDO) \/ tryptophan catabolism; IL-10; regulatory T-cells<\/p>\n Finding:<\/strong> Thymosin alpha 1 primed dendritic cells for Th1 resistance through TLR9 signalling and activated the immunosuppressive tryptophan-catabolism pathway via IDO; IDO activation required TLR9 and type I interferon-receptor signalling and resulted in IL-10 production and generation of regulatory T-cells \u2014 establishing a regulatory environment that balances inflammation and tolerance.<\/p>\n Website Claim:<\/strong> In preclinical models, thymosin alpha 1 has been studied in relation to dendritic-cell TLR9 signalling, IDO\/tryptophan catabolism, IL-10 and regulatory-T-cell induction (inflammation\u2013tolerance balance).<\/p>\n DOI: 10.1182\/blood-2006-02-004762 \u00b7 PMID: 16741252 \u00b7 URL: https:\/\/pubmed.ncbi.nlm.nih.gov\/16741252\/<\/p>\n Quelle:<\/strong> Bozza S, Gaziano R, Bonifazi P, Zelante T, Pitzurra L, Montagnoli C, Moretti S, Castronari R, Sinibaldi P, Rasi G, Garaci E, Bistoni F, Romani L, 2007, International Immunology<\/p>\n Research Area:<\/strong> Plasmacytoid dendritic-cell activation; TLR9 \/ MyD88 \/ IRF7 signalling; type I\/II interferon (IFN-\u03b1\/IFN-\u03b3) pathway<\/p>\n Finding:<\/strong> Thymosin alpha 1 protected susceptible and resistant mice from murine cytomegalovirus infection; the effect occurred through activation of plasmacytoid dendritic cells via TLR9\/MyD88-dependent viral sensing, leading to IRF7 activation and an IFN-\u03b1\/IFN-\u03b3-dependent effector pathway.<\/p>\n Website Claim:<\/strong> In preclinical models, thymosin alpha 1 has been studied in relation to plasmacytoid-dendritic-cell TLR9\/MyD88\/IRF7 signalling and the type I\/II interferon (IFN-\u03b1\/IFN-\u03b3) pathway.<\/p>\n DOI: 10.1093\/intimm\/dxm097 \u00b7 PMID: 17804687 \u00b7 URL: https:\/\/pubmed.ncbi.nlm.nih.gov\/17804687\/<\/p>\n Quelle:<\/strong> Huang Y, Chen Z, Zhou C, Yao H, Li M, Xu C, 2004, International Immunopharmacology<\/p>\n Research Area:<\/strong> Direct thymosin alpha 1 \u2013 dendritic-cell interaction; DC maturation\/differentiation; context-dependent IL-12 modulation<\/p>\n Finding:<\/strong> In the first reported example of a direct T\u03b11\u2013DC interaction, thymosin alpha 1 promoted CD4-expressing DC differentiation and up-regulated activation\/maturation markers on bone-marrow-derived dendritic cells; its effect on IL-12 production was context-dependent (modulated in the presence of TNF-\u03b1), indicating T\u03b11 can shape T-cell responses by acting at the DC level.<\/p>\n Website Claim:<\/strong> In vitro, thymosin alpha 1 has been studied for direct effects on dendritic-cell maturation, differentiation and activation-marker expression.<\/p>\n DOI: 10.1016\/j.intimp.2004.02.008 \u00b7 PMID: 15099531 \u00b7 URL: https:\/\/pubmed.ncbi.nlm.nih.gov\/15099531\/<\/p>\n Quelle:<\/strong> Bistoni F, Baccarini M, Puccetti P, Marconi P, Garaci E, 1984, Cancer Immunology, Immunotherapy<\/p>\n Research Area:<\/strong> Natural killer (NK) cell activity \/ cell-mediated cytotoxicity; thymic-factor immunomodulation<\/p>\n Finding:<\/strong> Administration of a thymic factor (thymostimulin, TP-1) markedly augmented NK-cell activity in mice; the abstract states the NK-boosting effect was also observed on administration of another thymic factor (thymosin alpha 1). The activated effectors were typical murine NK cells by functional\/antigenic criteria.<\/p>\n Website Claim:<\/strong> In preclinical research, thymosin alpha 1 has been studied among thymic factors in relation to natural killer (NK) cell activity.<\/p>\n DOI: 10.1007\/BF00205497 \u00b7 PMID: 6563944 \u00b7 URL: https:\/\/pubmed.ncbi.nlm.nih.gov\/6563944\/<\/p>\n Quelle:<\/strong> Romani L, Bistoni F, Montagnoli C, Gaziano R, Bozza S, Bonifazi P, Zelante T, Moretti S, Rasi G, Garaci E, Puccetti P, 2007, Annals of the New York Academy of Sciences<\/p>\n Research Area:<\/strong> Synthesis of the T\u03b11 immune mechanism: TLR signalling, dendritic cells, inflammation\u2013immunity\u2013tolerance balance<\/p>\n Finding:<\/strong> Review positioning thymosin alpha 1 as an endogenous regulator of inflammation, immunity and tolerance, integrating its TLR\/dendritic-cell signalling, Th1 priming and IDO-dependent regulatory effects into a single ‘balance’ framework.<\/p>\n Website Claim:<\/strong> Review literature positions thymosin alpha 1 as an endogenous regulator of inflammation, immunity and tolerance.<\/p>\n DOI: 10.1196\/annals.1415.002 \u00b7 PMID: 17495242 \u00b7 URL: https:\/\/pubmed.ncbi.nlm.nih.gov\/17495242\/<\/p>\n Quelle:<\/strong> King R, Tuthill C, 2016, Vitamins and Hormones<\/p>\n Research Area:<\/strong> Comprehensive review of T\u03b11 immune mechanism and pleiotropic action across immune-cell subsets<\/p>\n Finding:<\/strong> Review describing T\u03b11 as a peptide originally isolated for restoring immune function in thymectomized mice, with a pleiotropic mechanism: it acts through Toll-like receptors in both myeloid and plasmacytoid dendritic cells, activating signalling pathways and the production of immune-related cytokines, and affecting multiple immune-cell subsets; preclinical and clinical work is summarized.<\/p>\n Website Claim:<\/strong> Review literature describes thymosin alpha 1 as a pleiotropic immunomodulatory peptide acting through Toll-like receptors in dendritic cells and affecting multiple immune-cell subsets.<\/p>\n DOI: 10.1016\/bs.vh.2016.04.003 \u00b7 PMID: 27450734 \u00b7 URL: https:\/\/pubmed.ncbi.nlm.nih.gov\/27450734\/<\/p>\n Quelle:<\/strong> Wu J, Zhou L, Liu J, Ma G, Kou Q, He Z, Chen J, Ou-Yang B, Chen M, Li Y, Wu X, Gu B, Chen L, Zou Z, Qiang X, Chen Y, Lin A, Zhang G, Guan X, 2013, Critical Care<\/p>\n Research Area:<\/strong> Human immune-function research; monocyte HLA-DR (mHLA-DR) expression; immunomodulation in critical illness<\/p>\n Finding:<\/strong> In a 6-centre RCT in severe sepsis (361 patients), the T\u03b11 group showed significantly greater improvement in monocyte HLA-DR (mHLA-DR) at day 3 (mean difference 3.9%, 95% CI 0.2\u20137.6, P = 0.037) and day 7 (5.8%, 95% CI 1.0\u201310.5, P = 0.017). 28-day all-cause mortality was 26.0% (T\u03b11) vs 35.0% (control) \u2014 a marginal primary endpoint (RR 0.74, 95% CI 0.54\u20131.02; nonstratified P = 0.062; log-rank P = 0.049). No serious drug-related adverse events.<\/p>\n Website Claim:<\/strong> In clinical research, thymosin alpha 1 has been investigated in a randomized controlled trial in relation to a monocyte immune-function marker (HLA-DR) in critically ill patients.<\/p>\n DOI: 10.1186\/cc11932 \u00b7 PMID: 23327199 \u00b7 URL: https:\/\/pubmed.ncbi.nlm.nih.gov\/23327199\/<\/p>\n Quelle:<\/strong> Liu Y, Pan Y, Hu Z, Wu M, Wang C, Feng Z, Mao C, Tan Y, Liu Y, Chen L, Li M, Wang G, Yuan Z, Diao B, Wu Y, Chen Y, 2020, Clinical Infectious Diseases<\/p>\n Research Area:<\/strong> Human immune-function research; circulating CD4+\/CD8+ T-lymphocyte counts; T-cell exhaustion markers (PD-1, Tim-3); thymic output (TRECs)<\/p>\n Finding:<\/strong> In a retrospective review of 76 severe COVID-19 patients, T\u03b11 treatment was associated with enhanced blood T-cell numbers in patients with severe lymphocytopenia, restoration of CD8+\/CD4+ T-cell counts (notably in elderly patients), and reduced PD-1 and Tim-3 expression on CD8+ T cells, paralleling a rise in T-cell-receptor excision circles (TRECs, a thymic-output marker). Reduced mortality versus untreated was reported (11.11% vs 30.00%, P = 0.044).<\/p>\n Website Claim:<\/strong> In clinical research, thymosin alpha 1 has been investigated in relation to circulating T-lymphocyte counts and T-cell exhaustion markers (PD-1, Tim-3).<\/p>\n DOI: 10.1093\/cid\/ciaa630 \u00b7 PMID: 32442287 \u00b7 URL: https:\/\/pubmed.ncbi.nlm.nih.gov\/32442287\/<\/p>\n","protected":false},"excerpt":{"rendered":" Thymosin Alpha-1 ist kein generisches \u201eImmun-Peptid\u201c: Es ist ein sequenzdefiniertes 28-Aminos\u00e4uren-Thymuspeptid mit einer der am besten aufgekl\u00e4rten Wirkmechaniken der gesamten Peptidforschung. In Studien wurde gezeigt, dass T\u03b11 dendritische Zellen \u00fcber Toll-like-Rezeptoren (TLR9\/TLR2) und den MyD88 \u2192 NF-\u03baB \/ IRF7-Signalweg aktiviert \u2014 mit nachgeschalteten IL-12-, Interferon-(IFN-\u03b1\/IFN-\u03b3-) und Th1-Forschungs-Endpunkten. Die Studienlage reicht von der Erstcharakterisierung in PNAS (1977) \u00fcber zwei mechanistische Blood-Arbeiten bis zu humaner Immunfunktions-Forschung (z. B. Monozyten-HLA-DR, T-Zell-Marker). Kurz gesagt: T\u03b11 geh\u00f6rt zu den am breitesten charakterisierten immunmodulatorischen Forschungspeptiden \u00fcberhaupt \u2014 strikt study-framed. Nur f\u00fcr die Laborforschung \u2014 mit batch analytics-Dokumentation. Nicht f\u00fcr den human- oder veterin\u00e4rmedizinischen Gebrauch.<\/p>\n","protected":false},"featured_media":221,"comment_status":"open","ping_status":"closed","template":"","meta":[],"product_brand":[],"product_cat":[78,16],"product_tag":[],"class_list":["post-96","product","type-product","status-publish","has-post-thumbnail","product_cat-peptide-forschungszwecke","product_cat-regeneration-longevity","first","instock","taxable","shipping-taxable","purchasable","product-type-simple"],"jetpack_sharing_enabled":true,"_links":{"self":[{"href":"https:\/\/reborn-peptides.com\/en\/wp-json\/wp\/v2\/product\/96","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/reborn-peptides.com\/en\/wp-json\/wp\/v2\/product"}],"about":[{"href":"https:\/\/reborn-peptides.com\/en\/wp-json\/wp\/v2\/types\/product"}],"replies":[{"embeddable":true,"href":"https:\/\/reborn-peptides.com\/en\/wp-json\/wp\/v2\/comments?post=96"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/reborn-peptides.com\/en\/wp-json\/wp\/v2\/media\/221"}],"wp:attachment":[{"href":"https:\/\/reborn-peptides.com\/en\/wp-json\/wp\/v2\/media?parent=96"}],"wp:term":[{"taxonomy":"product_brand","embeddable":true,"href":"https:\/\/reborn-peptides.com\/en\/wp-json\/wp\/v2\/product_brand?post=96"},{"taxonomy":"product_cat","embeddable":true,"href":"https:\/\/reborn-peptides.com\/en\/wp-json\/wp\/v2\/product_cat?post=96"},{"taxonomy":"product_tag","embeddable":true,"href":"https:\/\/reborn-peptides.com\/en\/wp-json\/wp\/v2\/product_tag?post=96"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}2. Current status of thymosin research: evidence for the existence of a family of thymic factors that control T-cell maturation<\/h3>\n
3. Thymosin alpha 1 activates dendritic cells for antifungal Th1 resistance through toll-like receptor signaling<\/h3>\n
4. Thymosin alpha1 activates dendritic cell tryptophan catabolism and establishes a regulatory environment for balance of inflammation and tolerance<\/h3>\n
5. Thymosin alpha1 activates the TLR9\/MyD88\/IRF7-dependent murine cytomegalovirus sensing for induction of anti-viral responses in vivo<\/h3>\n
6. The modulation of thymosin alpha 1 in the maturation, differentiation and function of murine bone marrow-derived dendritic cells in the absence or presence of tumor necrosis factor-alpha<\/h3>\n
7. Enhancement of natural killer cell activity in mice by treatment with a thymic factor<\/h3>\n
8. Thymosin alpha1: an endogenous regulator of inflammation, immunity, and tolerance<\/h3>\n
9. Immune Modulation with Thymosin Alpha 1 Treatment<\/h3>\n
10. The efficacy of thymosin alpha 1 for severe sepsis (ETASS): a multicenter, single-blind, randomized and controlled trial<\/h3>\n
11. Thymosin Alpha 1 Reduces the Mortality of Severe Coronavirus Disease 2019 by Restoration of Lymphocytopenia and Reversion of Exhausted T Cells<\/h3>\n